NUTRIFLEX® OMEGA PLUS EMULSION FOR INFUSION

Alanine
Arginine
Aspartic Acid
Calcium Chloride Dihydrate
Glucose Monohydrate
Glutamic Acid
Glycine
Histidine Hydrochloride Monohydrate
Isoleucine
Leucine
Lysine
Magnesium Acetate Tetrahydrate
Methionine
Omega-3-Acid Triglycerides
Phenylalanine
Potassium Acetate
Proline
Serine
Sodium Acetate Trihydrate
Sodium Chloride
Sodium Dihydrogen Phosphate Dihydrate
Sodium Hydroxide
Soya-Bean Oil
Refined
Threonine
Triglycerides
Medium Chain
Tryptophan
Valine
Zinc Acetate Dihydrate

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.

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 |

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.

Pharmacodynamics

Is an important source of energy for muscle tissue, the brain and central nervous system; strengthens the immune system by producing antibodies; helps in the metabolism of sugars and organic acids.

Pharmacokinetics

Absorption:

Not Available

Distribution:

Not Available

Metabolism:

Not Available

Elimination:

Not Available

Half-life

Not Available

Clearance

Not Available

Toxicity

Not Available

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.

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 |

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.

Pharmacodynamics

Studies have shown that is has improved immune responses to bacteria, viruses and tumor cells; promotes wound healing and regeneration of the liver; causes the release of growth hormones; considered crucial for optimal muscle growth and tissue repair.

Pharmacokinetics

Absorption:

Absorbed from the lumen of the small intestine into the enterocytes. Absorption is efficient and occurs by an active transport mechanism.

Distribution:

Not Available

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:

Not Available

Half-life

Not Available

Clearance

Not Available

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.

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.

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 |

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.

Pharmacodynamics

L-aspartate is considered a non-essential amino acid, meaning that, under normal physiological conditions, sufficient amounts of the amino acid are synthesized in the body to meet the body's requirements. L-aspartate is formed by the transamination of the Krebs cycle intermediate oxaloacetate. The amino acid serves as a precursor for synthesis of proteins, oligopeptides, purines, pyrimidines, nucleic acids and L-arginine. L-aspartate is a glycogenic amino acid, and it can also promote energy production via its metabolism in the Krebs cycle. These latter activities were the rationale for the claim that supplemental aspartate has an anti-fatigue effect on skeletal muscle, a claim that was never confirmed.

Pharmacokinetics

Absorption:

Absorbed from the small intestine by an active transport process

Distribution:

Not Available

Metabolism:

Not Available

Elimination:

Not Available

Half-life

Not Available

Clearance

Not Available

Toxicity

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

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.

Active Ingredient / Synonyms

Not Available

Description

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Indication

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Mechanism of Action

Not Available

Pharmacodynamics

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Pharmacokinetics

Absorption:

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Distribution:

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Metabolism:

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Elimination:

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Half-life

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Clearance

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Toxicity

Not Available

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.

Active Ingredient / Synonyms

Not Available

Description

Not Available

Indication

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Mechanism of Action

Not Available

Pharmacodynamics

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Pharmacokinetics

Absorption:

Not Available

Distribution:

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Metabolism:

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Elimination:

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Half-life

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Clearance

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Toxicity

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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.

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 |

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.

Pharmacodynamics

Like other amino acids, glutamine is biochemically important as a constituent of proteins. Glutamine is also crucial in nitrogen metabolism. Ammonia (formed by nitrogen fixation) is assimilated into organic compounds by converting glutamic acid to glutamine. The enzyme which accomplishes this is called glutamine synthetase. Glutamine can then be used as a nitrogen donor in the biosynthesis of many compounds, including other amino acids, purines, and pyrimidines. L-glutamine improves nicotinamide adenine dinucleotide (NAD) redox potential [FDA Label].

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:

Primarily eliminated by metabolism [FDA Label]. While L-glutamine is filtered though the glomerulus, nearly all is reabsorbed by renal tubules.

Half-life

The half life of elimination is 1 h [FDA Label].

Clearance

Not Available

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].

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.

Active Ingredient / Synonyms

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

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.

Pharmacodynamics

Helps trigger the release of oxygen to the energy requiring cell-making process; Important in the manufacturing of hormones responsible for a strong immune system.

Pharmacokinetics

Absorption:

Absorbed from the small intestine via an active transport mechanism.

Distribution:

Not Available

Metabolism:

Hepatic

Elimination:

Not Available

Half-life

Not Available

Clearance

Not Available

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.

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.

Active Ingredient / Synonyms

Not Available

Description

Not Available

Indication

Not Available

Mechanism of Action

Not Available

Pharmacodynamics

Not Available

Pharmacokinetics

Absorption:

Not Available

Distribution:

Not Available

Metabolism:

Not Available

Elimination:

Not Available

Half-life

Not Available

Clearance

Not Available

Toxicity

Not Available

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.

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 |

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.

Pharmacodynamics

They provide ingredients for the manufacturing of other essential biochemical components in the body, some of which are utilized for the production of energy, stimulants to the upper brain and helping you to be more alert.

Pharmacokinetics

Absorption:

Absorbed from the small intestine by a sodium-dependent active-transport process

Distribution:

Not Available

Metabolism:

Hepatic

Elimination:

Not Available

Half-life

Not Available

Clearance

Not Available

Toxicity

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

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.

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 |

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.

Pharmacodynamics

An essential amino acid. (Claim) Leucine helps with the regulation of blood-sugar levels, the growth and repair of muscle tissue (such as bones, skin and muscles), growth hormone production, wound healing as well as energy regulation. It can assist to prevent the breakdown of muscle proteins that sometimes occur after trauma or severe stress. It may also be beneficial for individuals with phenylketonuria - a condition in which the body cannot metabolize the amino acid phenylalanine

Pharmacokinetics

Absorption:

Not Available

Distribution:

Not Available

Metabolism:

Not Available

Elimination:

Not Available

Half-life

Not Available

Clearance

Not Available

Toxicity

Not Available

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.

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 |

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.

Pharmacodynamics

Insures the adequate absorption of calcium; helps form collagen ( which makes up bone cartilage & connective tissues); aids in the production of antibodies, hormones & enzymes. Recent studies have shown that Lysine may be effective against herpes by improving the balance of nutrients that reduce viral growth. A deficiency may result in tiredness, inability to concentrate, irritability, bloodshot eyes, retarded growth, hair loss, anemia & reproductive problems.

Pharmacokinetics

Absorption:

Absorbed from the lumen of the small intestine into the enterocytes by an active transport process

Distribution:

Not Available

Metabolism:

Hepatic

Elimination:

Not Available

Half-life

Not Available

Clearance

Not Available

Toxicity

Not Available

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.

Active Ingredient / Synonyms

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

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.

Pharmacodynamics

Magnesium is an essential cofactor for many enzymatic reactions such as protein synthesis and ATP production. It also participates in adenylyl cyclase pathway and tyrosine kinase signalling pathways. Magnesium may also play a role in regulating glucose metabolism. It serves as an essential cation for a number of biochemical processes involved in nerve signaling, bone mineralization and muscle contractions.

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:

Not Available

Elimination:

Mainly renal exctretion, where up to 97% of magnesium may be excreted renally during hypermagnesemia.

Half-life

Elimination half-life has been reported to be 27.7 hours following an overdose of 400mEq magnesium in an adult.

Clearance

Not Available

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.

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.

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 |

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.

Pharmacodynamics

L-Methionine is a principle supplier of sulfur which prevents disorders of the hair, skin and nails; helps lower cholesterol levels by increasing the liver's production of lecithin; reduces liver fat and protects the kidneys; a natural chelating agent for heavy metals; regulates the formation of ammonia and creates ammonia-free urine which reduces bladder irritation; influences hair follicles and promotes hair growth. L-methionine may protect against the toxic effects of hepatotoxins, such as acetaminophen. Methionine may have antioxidant activity.

Pharmacokinetics

Absorption:

Absorbed from the lumen of the small intestine into the enterocytes by an active transport process.

Distribution:

Not Available

Metabolism:

Hepatic

Elimination:

Not Available

Half-life

Not Available

Clearance

Not Available

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.

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.

Active Ingredient / Synonyms

Not Available

Description

Not Available

Indication

Not Available

Mechanism of Action

Not Available

Pharmacodynamics

Not Available

Pharmacokinetics

Absorption:

Not Available

Distribution:

Not Available

Metabolism:

Not Available

Elimination:

Not Available

Half-life

Not Available

Clearance

Not Available

Toxicity

Not Available

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.

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 |

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

Pharmacodynamics

Used by the brain to produce Norepinephrine, a chemical that transmits signals between nerve cells and the brain; keeps you awake and alert; reduces hunger pains; functions as an antidepressant and helps improve memory.

Pharmacokinetics

Absorption:

Absorbed from the small intestine by a sodium dependent active transport process.

Distribution:

Not Available

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:

Not Available

Half-life

Not Available

Clearance

Not Available

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.

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.

Active Ingredient / Synonyms

Not Available

Description

Not Available

Indication

Not Available

Mechanism of Action

Not Available

Pharmacodynamics

Not Available

Pharmacokinetics

Absorption:

Not Available

Distribution:

Not Available

Metabolism:

Not Available

Elimination:

Not Available

Half-life

Not Available

Clearance

Not Available

Toxicity

Not Available

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.

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 |

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.

Pharmacodynamics

L-Proline is a major amino acid found in cartilage and is important for maintaining youthful skin as well as repair of muscle, connective tissue and skin damage. It is also essential for the immune system, and for necessary balance of this formula. It is an essential component of collagen and is important for proper functioning of joints and tendons. L-Proline is extremely important for the proper functioning of joints and tendons. Helps maintain and strengthen heart muscles.

Pharmacokinetics

Absorption:

Not Available

Distribution:

Not Available

Metabolism:

Hepatic

Elimination:

Not Available

Half-life

Not Available

Clearance

Not Available

Toxicity

Not Available

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.

Active Ingredient / Synonyms

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

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.

Pharmacodynamics

Serine is classified as a nutritionally non-essential amino acid. Serine is critical for the production of the body's proteins, enzymes and muscle tissue. Serine is needed for the proper metabolism of fats and fatty acids. It also helps in the production of antibodies. Serine is used as a natural moisturizing agent in some cosmetics and skin care products. The main source of essential amino acids is from the diet, non-essential amino acids are normally synthesize by humans and other mammals from common intermediates.

Pharmacokinetics

Absorption:

Not Available

Distribution:

Not Available

Metabolism:

Not Available

Elimination:

Not Available

Half-life

Not Available

Clearance

Not Available

Toxicity

Not Available

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.

Active Ingredient / Synonyms

Not Available

Description

Not Available

Indication

Not Available

Mechanism of Action

Not Available

Pharmacodynamics

Not Available

Pharmacokinetics

Absorption:

Not Available

Distribution:

Not Available

Metabolism:

Not Available

Elimination:

Not Available

Half-life

Not Available

Clearance

Not Available

Toxicity

Not Available

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.

Active Ingredient / Synonyms

Sodium Chloride | Sodium Chloride |

Description

Sodium chloride, also known as salt, common salt, table salt or halite, is an ionic compound with the chemical formula NaCl, representing a 1:1 ratio of sodium and chloride ions. Sodium chloride is the salt most responsible for the salinity of seawater and of the extracellular fluid of many multicellular organisms. It is listed on the World Health Organization Model List of Essential Medicines.

Indication

This intravenous solution is indicated for use in adults and pediatric patients as a source of electrolytes and water for hydration. Also, designed for use as a diluent and delivery system for intermittent intravenous administration of compatible drug additives.

Mechanism of Action

Sodium and chloride — major electrolytes of the fluid compartment outside of cells (i.e., extracellular) — work together to control extracellular volume and blood pressure. Disturbances in sodium concentrations in the extracellular fluid are associated with disorders of water balance.

Pharmacodynamics

Sodium, the major cation of the extracellular fluid, functions primarily in the control of water distribution, fluid balance, and osmotic pressure of body fluids. Sodium is also associated with chloride and bicarbonate in the regulation of the acid-base equilibrium of body fluid. Chloride, the major extracellular anion, closely follows the metabolism of sodium, and changes in the acid-base balance of the body are reflected by changes in the chloride concentration.

Pharmacokinetics

Absorption:

Absorption of sodium in the small intestine plays an important role in the absorption of chloride, amino acids, glucose, and water. Chloride, in the form of hydrochloric acid (HCl), is also an important component of gastric juice, which aids the digestion and absorption of many nutrients.

Distribution:

The volume of distribution is 0.64 L/kg.

Metabolism:

The salt that is taken in to gastro intestinal tract remains for the most part unabsorbed as the liquid contents pass through the stomach and small bowel. On reaching the colon this salt, together with the water is taken in to the blood. As excesses are absorbed the kidney is constantly excreting sodium chloride, so that the chloride level in the blood and tissues remains fairly constant.Further more, if the chloride intake ceases, the kidney ceases to excrete chlorides. Body maintains an equilibrium retaining the 300gm of salt dissolved in the blood and fluid elements of the tissue dissociated into sodium ions and chloride ions.

Elimination:

Substantially excreted by the kidneys. (drugs.com)

Half-life

17 minutes ( wikipedia)

Clearance

Not Available

Toxicity

The rare inadvertent intravascular administration or rapid intravascular absorption of hypertonic sodium chloride can cause a shift of tissue fluids into the vascular bed, resulting in hypervolemia, electrolyte disturbances, circulatory failure, pulmonary embolism, or augmented hypertension. ( toxnet)

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.

Active Ingredient / Synonyms

Not Available

Description

Not Available

Indication

Not Available

Mechanism of Action

Not Available

Pharmacodynamics

Not Available

Pharmacokinetics

Absorption:

Not Available

Distribution:

Not Available

Metabolism:

Not Available

Elimination:

Not Available

Half-life

Not Available

Clearance

Not Available

Toxicity

Not Available

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.

Active Ingredient / Synonyms

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

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].

Pharmacodynamics

Sodium Hydroxide 10% forms a strongly alkaline and caustic solution. As a caustic agent, it is used to destroy organic tissue by chemical action [L1968].

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:

Not Available

Metabolism:

Not Available

Elimination:

Not Available

Half-life

Not Available

Clearance

Not Available

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].

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.

Active Ingredient / Synonyms

Not Available

Description

Not Available

Indication

Not Available

Mechanism of Action

Not Available

Pharmacodynamics

Not Available

Pharmacokinetics

Absorption:

Not Available

Distribution:

Not Available

Metabolism:

Not Available

Elimination:

Not Available

Half-life

Not Available

Clearance

Not Available

Toxicity

Not Available

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.

Active Ingredient / Synonyms

Not Available

Description

Not Available

Indication

Not Available

Mechanism of Action

Not Available

Pharmacodynamics

Not Available

Pharmacokinetics

Absorption:

Not Available

Distribution:

Not Available

Metabolism:

Not Available

Elimination:

Not Available

Half-life

Not Available

Clearance

Not Available

Toxicity

Not Available

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.

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 |

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.

Pharmacodynamics

L-Threonine is an essential amino acid that helps to maintain the proper protein balance in the body. It is important for the formation of collagen, elastin, and tooth enamel, and aids liver and lipotropic function when combined with aspartic acid and methionine.

Pharmacokinetics

Absorption:

Not Available

Distribution:

Not Available

Metabolism:

Hepatic

Elimination:

Not Available

Half-life

Not Available

Clearance

Not Available

Toxicity

Not Available

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.

Active Ingredient / Synonyms

Caprylic/capric triglyceride | Caprylic/capric triglycerides | Coconut oil, fractioned | Fractionated coconut oil | Fractionated triglyceride of coconut oil | MCT | Medium chain triglyceride | Medium-chain glycerides | Triglycerides, medium-chain | Medium-chain triglycerides |

Description

Compared to long-chain fatty acids which are dietary fats that are composed of 2 to 22 carbon atoms in length, medium-chain triglycerides (MCTs) are composed of only 6 to 12 carbon links [F126, F128]. This shorter chain length gives MCTs properties that are unique, and perhaps pharmacologically advantageous over long-chain fatty acids [F128, F126]. In essence, the shorter chain length chemical profile of MCTs allow them to passively and directly diffuse across the gastrointestinal tract into the portal system without undergoing the prolonged and necessary sequential molecular modifications that long-chain fatty acids must undertake [F128, F126]. These kinds of pharmacodynamics ultimately allow for much quicker absorption and utilization of MCTs compared to long-chain triglycerides - making them important and rapid sources of calories and essential fatty acids for various medical conditions associated with malnutrition and malabsorption [F126, F128].

Indication

When incorporated as an active ingredient in combination with other active components like fish oils, soya oil, and olive oil as a prescription medication (SMOFLIPID), medium chain triglycerides (MCTs) constitute a therapy indicated for supplying energy, calories, and essential fatty acids to adult patients, as part of a parenteral nutrition regimen, when oral or enteral nutrition is impossible, insufficient, or contraindicated [F126, F127]. However, given the predominant indication of MCTs for acting as a source of calories and essential fatty acids, the use of MCTs alone or as a component part of various unique, individual patient-tailored composite regimen therapies, MCTs are also ultimately indicated for a wide range of health conditions that involve energy deficiency, malnutrition, or disturbances in the ordinary absorption of dietary fats [A33175, F128]. Such conditions can include Crohn's disease, Waldmann disease, weight maintenance in AIDS, cachexia, and various disturbances in patient bile secretion (like cholestasis, disturbances in hepatic-intestinal circulation of bile acids, intestinal dysbacteriosis), or in pancreatic lipase secretion (like pancreatic failure in the course of cystic fibrosis) [A33175, F128].

Mechanism of Action

Absorption of larger long-chain triglycerides (LCT) requires specific processing in the digestive tract, like emulsification with bile [A33175]. This process is aimed at obtaining the maximum surface for digestion (lipolysis with breakage of ester bonds of triglycerides and with the release of monoglycerides, free fatty acids, and glycerol) [A33175]. The process of digestion of fats occurs largely in the duodenum and initial segment of the jejunum [A33175]. Lipases are found in the pancreatic juice and the brush border [A33175]. Once the aforementioned bonds are broken and the fatty acids and monoglycerides are absorbed into an enterocyte, they undergo resynthesis to triglycerides, in the presence of ligase, co-enzyme A, and ATP. Chylomicrons are formed. They get to the lymph and only then can they be transported to blood and destination organs [A33175]. Release of fats from chylomicrons requires the presence of plasmatic lipases, and only then can they be metabolised or stored as a reserve in the fatty tissue [A33175]. Conversely, hydrolysis of medium chain triglycerides (MCTs, which is faster than LCT hydrolysis anyway) does not require bile and lipase [A33175]. Without hydrolysis, they may also be absorbed by the enterocytes and they do not require re-esterification [A33175]. From enterocytes they are directly absorbed into the portal vein and then transported mainly to the liver. Thus, absorption of MCT is faster than that of LCTs [A33175]. Their metabolism is facilitated as well because they are metabolised by the liver almost completely (only when the liver’s metabolic abilities are exceeded the process is taken over by peripheral tissues) with energy release, regardless of the presence of carnitine (which is necessary for the transport of long-chain fatty acids through the mitochondrial membrane) [A33175]. Thanks to this the availability of medium-chain fatty acids for mitochondrial oxidation is better [A33175]. This means that MCT are an easy and quick source of energy [A33175]. However, it should be borne in mind that quantities of MCT exceeding the abilities of the liver are metabolised peripherally in a carnitine-dependent mechanism, which can increase the demand for it [A33175]. On the other hand, it has been observed that on the enterohormonal pathway (an important element of which is a MCT-induced increase of the YY peptide concentration and a decrease in cholecystokinin release) MCT cause a decrease of appetite and consequently a decrease in energy intake [A33175]. They also interfere with the metabolism of the fatty tissue, by hindering the creation of a deposit from long chain acids [A33175]. It has been proven that an MCT-enriched diet modulates metabolism of fats, which is manifested as a decrease in the concentration of triglycerides and cholesterol [A33175]. Moreover, unlike LCT, MCT do not affect the release of cholecystokinin or the emptying of the gallbladder and they do not increase the secretion of pancreatic enzymes [A33175]. They can speed up the intestinal passage by affecting the release of the YY peptide, but only in the distal sections of the intestine [A33175]. Moreover, it has been found that MCT facilitate absorption of calcium [A33175].

Pharmacodynamics

Medium chain triglycerides (MCTs) are considered a fast acting source of calories and essential fatty acids for patients with malnutrition, malabsorption, or particular fatty-acid metabolism disorders because they can passively and directly diffuse across the gastrointestinal tract into the portal system without undergoing the prolonged and necessary sequential molecular modifications that long-chain fatty acids must undertake [F126]. These kinds of pharmacodynamics allow for much quicker absorption and utilization of MCTs compared to long-chain triglycerides [F128]. In contrast, albumin-bound long-chain fatty acids do not readily enter peripheral organs and are predominantly metabolised by the liver with a preference for re-esterification to phospholipids or triglycerides and therefore potentially fat storage [F126]. MCFAs are subjected to a lower re-esterification rate than LCFAs with a reduced tendency to fat storage than LCTs [F126]. Subsequently, MCTs are predominantly catabolized, rather than stored as adipose tissue and are therefore utilized as an immediate source of energy, considering it does not require energy to absorb, use, or store MCTs [F126].

Pharmacokinetics

Absorption:

The absorption of medium chain triglycerides is considered rapid [A33175, L2895, F126, F127, F128] but that both long-chain triglycerides and medium chain triglycerides share a similar absorption, which is an absorption rate of about 95% - similar to that of other ingested fats [L784].

Distribution:

The apparent volumes of distribution have been researched as approximately 4.5 L for medium chain triglycerides and 19 L for medium chain fatty acids in a typical 70-kg subject [A33174].

Metabolism:

In capillaries, both medium chain triglycerides (MCTs) and long-chain triglycerides (LCTs) are hydrolysed by lipoprotein lipase to glycerol and free fatty acids, and medium chain fatty acids (MCFAs) and long chain fatty acids (LCFAs), respectively [F126]. MCTs are hydrolysed at a faster rate than LCTs and therefore have a faster elimination rate [F126]. Free MCFAs then readily enter the liver, kidney, heart and other peripheral organs where they are oxidised by β-oxidation and the citric acid cycle to carbon dioxide and water [F126]. Alternatively, via the ketogenesis pathway, the β-oxidation of fatty acids generates the acetyl-CoA that can lead to the formation of ketone bodies like acetoacetate and β-hydroxybutyrate [F126].

Elimination:

Readily accessible data regarding the route of elimination of medium chain fatty acids is not available.

Half-life

The plasma half-life of medium chain triglycerides is recorded to be 11 minutes and that of medium chain fatty acids is about 17 minutes [A33174].

Clearance

The clearance of medium chain triglycerides in healthy control subjects was measured to be about 1.93 +/- 0.34 mL.kg-1.min-1 [A33179].

Toxicity

The excess use of medium chain triglycerides (MCTs) can lead to increased plasma levels of medium chain dicarboxylic acids, 3-hydroxy fatty acids and ketone bodies [F126]. Hyperketonaemia was observed in repeat-dose toxicity studies with SMOFLIPID [F126]. If excess MCTs are administered, the capacity of extrahepatic tissues to use ketone bodies is saturated and this may be of particular concern in some diabetes patients [F126]. The increased level of ketone bodies aggravates metabolic acidosis and accelerates the breakdown of homeostatic mechanisms [F126].

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.

Active Ingredient / Synonyms

Caprylic/capric triglyceride | Caprylic/capric triglycerides | Coconut oil, fractioned | Fractionated coconut oil | Fractionated triglyceride of coconut oil | MCT | Medium chain triglyceride | Medium-chain glycerides | Triglycerides, medium-chain | Medium-chain triglycerides |

Description

Compared to long-chain fatty acids which are dietary fats that are composed of 2 to 22 carbon atoms in length, medium-chain triglycerides (MCTs) are composed of only 6 to 12 carbon links [F126, F128]. This shorter chain length gives MCTs properties that are unique, and perhaps pharmacologically advantageous over long-chain fatty acids [F128, F126]. In essence, the shorter chain length chemical profile of MCTs allow them to passively and directly diffuse across the gastrointestinal tract into the portal system without undergoing the prolonged and necessary sequential molecular modifications that long-chain fatty acids must undertake [F128, F126]. These kinds of pharmacodynamics ultimately allow for much quicker absorption and utilization of MCTs compared to long-chain triglycerides - making them important and rapid sources of calories and essential fatty acids for various medical conditions associated with malnutrition and malabsorption [F126, F128].

Indication

When incorporated as an active ingredient in combination with other active components like fish oils, soya oil, and olive oil as a prescription medication (SMOFLIPID), medium chain triglycerides (MCTs) constitute a therapy indicated for supplying energy, calories, and essential fatty acids to adult patients, as part of a parenteral nutrition regimen, when oral or enteral nutrition is impossible, insufficient, or contraindicated [F126, F127]. However, given the predominant indication of MCTs for acting as a source of calories and essential fatty acids, the use of MCTs alone or as a component part of various unique, individual patient-tailored composite regimen therapies, MCTs are also ultimately indicated for a wide range of health conditions that involve energy deficiency, malnutrition, or disturbances in the ordinary absorption of dietary fats [A33175, F128]. Such conditions can include Crohn's disease, Waldmann disease, weight maintenance in AIDS, cachexia, and various disturbances in patient bile secretion (like cholestasis, disturbances in hepatic-intestinal circulation of bile acids, intestinal dysbacteriosis), or in pancreatic lipase secretion (like pancreatic failure in the course of cystic fibrosis) [A33175, F128].

Mechanism of Action

Absorption of larger long-chain triglycerides (LCT) requires specific processing in the digestive tract, like emulsification with bile [A33175]. This process is aimed at obtaining the maximum surface for digestion (lipolysis with breakage of ester bonds of triglycerides and with the release of monoglycerides, free fatty acids, and glycerol) [A33175]. The process of digestion of fats occurs largely in the duodenum and initial segment of the jejunum [A33175]. Lipases are found in the pancreatic juice and the brush border [A33175]. Once the aforementioned bonds are broken and the fatty acids and monoglycerides are absorbed into an enterocyte, they undergo resynthesis to triglycerides, in the presence of ligase, co-enzyme A, and ATP. Chylomicrons are formed. They get to the lymph and only then can they be transported to blood and destination organs [A33175]. Release of fats from chylomicrons requires the presence of plasmatic lipases, and only then can they be metabolised or stored as a reserve in the fatty tissue [A33175]. Conversely, hydrolysis of medium chain triglycerides (MCTs, which is faster than LCT hydrolysis anyway) does not require bile and lipase [A33175]. Without hydrolysis, they may also be absorbed by the enterocytes and they do not require re-esterification [A33175]. From enterocytes they are directly absorbed into the portal vein and then transported mainly to the liver. Thus, absorption of MCT is faster than that of LCTs [A33175]. Their metabolism is facilitated as well because they are metabolised by the liver almost completely (only when the liver’s metabolic abilities are exceeded the process is taken over by peripheral tissues) with energy release, regardless of the presence of carnitine (which is necessary for the transport of long-chain fatty acids through the mitochondrial membrane) [A33175]. Thanks to this the availability of medium-chain fatty acids for mitochondrial oxidation is better [A33175]. This means that MCT are an easy and quick source of energy [A33175]. However, it should be borne in mind that quantities of MCT exceeding the abilities of the liver are metabolised peripherally in a carnitine-dependent mechanism, which can increase the demand for it [A33175]. On the other hand, it has been observed that on the enterohormonal pathway (an important element of which is a MCT-induced increase of the YY peptide concentration and a decrease in cholecystokinin release) MCT cause a decrease of appetite and consequently a decrease in energy intake [A33175]. They also interfere with the metabolism of the fatty tissue, by hindering the creation of a deposit from long chain acids [A33175]. It has been proven that an MCT-enriched diet modulates metabolism of fats, which is manifested as a decrease in the concentration of triglycerides and cholesterol [A33175]. Moreover, unlike LCT, MCT do not affect the release of cholecystokinin or the emptying of the gallbladder and they do not increase the secretion of pancreatic enzymes [A33175]. They can speed up the intestinal passage by affecting the release of the YY peptide, but only in the distal sections of the intestine [A33175]. Moreover, it has been found that MCT facilitate absorption of calcium [A33175].

Pharmacodynamics

Medium chain triglycerides (MCTs) are considered a fast acting source of calories and essential fatty acids for patients with malnutrition, malabsorption, or particular fatty-acid metabolism disorders because they can passively and directly diffuse across the gastrointestinal tract into the portal system without undergoing the prolonged and necessary sequential molecular modifications that long-chain fatty acids must undertake [F126]. These kinds of pharmacodynamics allow for much quicker absorption and utilization of MCTs compared to long-chain triglycerides [F128]. In contrast, albumin-bound long-chain fatty acids do not readily enter peripheral organs and are predominantly metabolised by the liver with a preference for re-esterification to phospholipids or triglycerides and therefore potentially fat storage [F126]. MCFAs are subjected to a lower re-esterification rate than LCFAs with a reduced tendency to fat storage than LCTs [F126]. Subsequently, MCTs are predominantly catabolized, rather than stored as adipose tissue and are therefore utilized as an immediate source of energy, considering it does not require energy to absorb, use, or store MCTs [F126].

Pharmacokinetics

Absorption:

The absorption of medium chain triglycerides is considered rapid [A33175, L2895, F126, F127, F128] but that both long-chain triglycerides and medium chain triglycerides share a similar absorption, which is an absorption rate of about 95% - similar to that of other ingested fats [L784].

Distribution:

The apparent volumes of distribution have been researched as approximately 4.5 L for medium chain triglycerides and 19 L for medium chain fatty acids in a typical 70-kg subject [A33174].

Metabolism:

In capillaries, both medium chain triglycerides (MCTs) and long-chain triglycerides (LCTs) are hydrolysed by lipoprotein lipase to glycerol and free fatty acids, and medium chain fatty acids (MCFAs) and long chain fatty acids (LCFAs), respectively [F126]. MCTs are hydrolysed at a faster rate than LCTs and therefore have a faster elimination rate [F126]. Free MCFAs then readily enter the liver, kidney, heart and other peripheral organs where they are oxidised by β-oxidation and the citric acid cycle to carbon dioxide and water [F126]. Alternatively, via the ketogenesis pathway, the β-oxidation of fatty acids generates the acetyl-CoA that can lead to the formation of ketone bodies like acetoacetate and β-hydroxybutyrate [F126].

Elimination:

Readily accessible data regarding the route of elimination of medium chain fatty acids is not available.

Half-life

The plasma half-life of medium chain triglycerides is recorded to be 11 minutes and that of medium chain fatty acids is about 17 minutes [A33174].

Clearance

The clearance of medium chain triglycerides in healthy control subjects was measured to be about 1.93 +/- 0.34 mL.kg-1.min-1 [A33179].

Toxicity

The excess use of medium chain triglycerides (MCTs) can lead to increased plasma levels of medium chain dicarboxylic acids, 3-hydroxy fatty acids and ketone bodies [F126]. Hyperketonaemia was observed in repeat-dose toxicity studies with SMOFLIPID [F126]. If excess MCTs are administered, the capacity of extrahepatic tissues to use ketone bodies is saturated and this may be of particular concern in some diabetes patients [F126]. The increased level of ketone bodies aggravates metabolic acidosis and accelerates the breakdown of homeostatic mechanisms [F126].

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.

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 |

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+.

Pharmacodynamics

Tryptophan is critical for the production of the body's proteins, enzymes and muscle tissue. It is also essential for the production of niacin, the synthesis of the neurotransmitter serotonin and melatonin. Tryptophan supplements can be used as natural relaxants to help relieve insomnia. Tryptophan can also reduce anxiety and depression and has been shown to reduce the intensity of migraine headaches. Other promising indications include the relief of chronic pain, reduction of impulsivity or mania and the treatment of obsessive or compulsive disorders. Tryptophan also appears to help the immune system and can reduce the risk of cardiac spasms. Tryptophan deficiencies may lead to coronary artery spasms. Tryptophan is used as an essential nutrient in infant formulas and intravenous feeding. Tryptophan is marketed as a prescription drug (Tryptan) for those who do not seem to respond well to conventional antidepressants. It may also be used to treat those afflicted with seasonal affective disorder (a winter-onset depression). Tryptopan serves as the precursor for the synthesis of serotonin (5-hydroxytryptamine, 5-HT) and melatonin (N-acetyl-5-methoxytryptamine).

Pharmacokinetics

Absorption:

Not Available

Distribution:

Not Available

Metabolism:

Hepatic.

Elimination:

Not Available

Half-life

Not Available

Clearance

Not Available

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.

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.

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 |

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.

Pharmacodynamics

L-valine is a branched-chain essential amino acid (BCAA) that has stimulant activity. It promotes muscle growth and tissue repair. It is a precursor in the penicillin biosynthetic pathway. Valine is one of three branched-chain amino acids (the others are leucine and isoleucine) that enhance energy, increase endurance, and aid in muscle tissue recovery and repair. This group also lowers elevated blood sugar levels and increases growth hormone production. Supplemental valine should always be combined with isoleucine and leucine at a respective milligram ratio of 2:1:2. It is an essential amino acid found in proteins; important for optimal growth in infants and for growth in children and nitrogen balance in adults. The lack of L-valine may influence the growth of body, cause neuropathic obstacle, anaemia. It has wide applications in the field of pharmaceutical and food industry.

Pharmacokinetics

Absorption:

Absorbed from the small intestine by a sodium-dependent active-transport process.

Distribution:

Not Available

Metabolism:

Hepatic

Elimination:

Not Available

Half-life

Not Available

Clearance

Not Available

Toxicity

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

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.

Active Ingredient / Synonyms

Not Available

Description

Not Available

Indication

Not Available

Mechanism of Action

Not Available

Pharmacodynamics

Not Available

Pharmacokinetics

Absorption:

Not Available

Distribution:

Not Available

Metabolism:

Not Available

Elimination:

Not Available

Half-life

Not Available

Clearance

Not Available

Toxicity

Not Available

References

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

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Approval Information

NUTRIFLEX OMEGA PLUS EMULSION FOR INFUSION was registered with Health Science Authority of Singapore by B. BRAUN SINGAPORE PTE LTD. It is marketed with the registration number of SIN15468P with effective from 2018-04-23.

This product contains 4.656g/1000ml of Alanine,2.592g/1000ml of Arginine,1.440g/1000ml of Aspartic Acid,0.470g/1000ml of Calcium Chloride Dihydrate,132.0g/1000ml of Glucose Monohydrate,3.368g/1000ml of Glutamic Acid,1.584g/1000ml of Glycine,1.624g/1000ml of Histidine Hydrochloride Monohydrate,2.256g/1000ml of Isoleucine,3.008g/1000ml of Leucine,2.728g/1000ml of Lysine,0.686g/1000ml of Magnesium Acetate Tetrahydrate,1.880g/1000ml of Methionine,4.00g/1000ml of Omega-3-Acid Triglycerides,3.368g/1000ml of Phenylalanine,2.747g/1000ml of Potassium Acetate,3.264g/1000ml of Proline,2.880g/1000ml of Serine,0.222g/1000ml of Sodium Acetate Trihydrate,0.402g/1000ml of Sodium Chloride,1.872g/1000ml of Sodium Dihydrogen Phosphate Dihydrate,0.781g/1000ml of Sodium Hydroxide,16.00g/1000ml of Soya-Bean Oil,1.744g/1000ml of Refined,20.00g/1000ml of Threonine,0.544g/1000ml of Triglycerides,2.496g/1000ml of Medium Chain,5.264mg/1000ml of Tryptophan, of Valine, and of Zinc Acetate Dihydrate in the form of INJECTION, EMULSION.

The medicine was manufactured by B. Braun Melsungen AG in GERMANY

It is a Presciption Only Medicine which can only be obtained from a doctor or a dentist, or from a pharmacist with a prescription from a Singapore-registered doctor or dentist.

Anatomical Therapeutic Chemical (ATC) Classification

ATC Code: B05BA10

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22 ZENMOLIN SYRUP 2mg/5ml Salbutamol P Only DRUG HOUSES OF AUSTRALIA PTE LTD Active
41 APO-PROPRANOLOL TABLET 40mg Propranolol POM PHARMAFORTE SINGAPORE PTE LTD Active
42 APO-DIAZEPAM TABLET 2mg Diazepam POM PHARMAFORTE SINGAPORE PTE LTD Active
44 APO-DIAZEPAM TABLET 5mg Diazepam POM PHARMAFORTE SINGAPORE PTE LTD Active
45 APO-DIAZEPAM TABLET 10mg Diazepam POM PHARMAFORTE SINGAPORE PTE LTD Active
46 APO-PROPRANOLOL TABLET 10mg Propranolol POM PHARMAFORTE SINGAPORE PTE LTD Active
55 APO-ISDN TABLET 10mg Isosorbide Dinitrate POM PHARMAFORTE SINGAPORE PTE LTD Active
63 DIAPO TABLET 10mg Diazepam POM BEACONS PHARMACEUTICALS PTE LTD Active
64 FURMIDE TABLET 40mg Furosemide POM BEACONS PHARMACEUTICALS PTE LTD Active

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5 DIPHENHYDRAMINE EXPECTORANT PAED. Ammonium Chloride|Diphenhydramine|Sodium Citrate P Only DRUG HOUSES OF AUSTRALIA PTE LTD Active
400 FAKTU SUPPOSITORY Cinchocaine|Policresulen P Only TAKEDA PHARMACEUTICALS (ASIA PACIFIC) PTE LTD Active
407 TRIMAXAZOLE TABLET Sulfamethoxazole|Trimethoprim POM BEACONS PHARMACEUTICALS PTE LTD Active
435 APO-SULFATRIM TABLET Sulfamethoxazole|Trimethoprim POM PHARMAFORTE SINGAPORE PTE LTD Active
508 APO-SULFATRIM PEDIATRIC TABLET Sulfamethoxazole|Trimethoprim POM PHARMAFORTE SINGAPORE PTE LTD Active
526 B.S. SUSPENSION Sulfamethoxazole|Trimethoprim POM APEX PHARMA MARKETING PTE LTD Active
583 CO-TRIMEXAZOLE SUSPENSION Sulfamethoxazole|Trimethoprim POM BEACONS PHARMACEUTICALS PTE LTD Active
676 BANEOCIN OINTMENT Bacitracin|Neomycin POM NOVARTIS (SINGAPORE) PTE LTD Active
678 BANEOCIN POWDER Bacitracin|Neomycin POM NOVARTIS (SINGAPORE) PTE LTD Active
706 TIENAM 500 FOR INJECTION Imipenem|Cilastatin POM MSD PHARMA (SINGAPORE) PTE LTD Active