Product Information
Registration Status: ActiveSIN05207P
VITALIPID N INFANT INJECTION is approved to be sold in Singapore with effective from 1990-11-14. It is marketed by FRESENIUS KABI (SINGAPORE) PTE LTD, with the registration number of SIN05207P.
This product contains Vitamin A 230 iu/ml,Vitamin D2 40 iu/ml,Vitamin E 0.7 iu/ml, and Vitamin K1 20mcg/ml in the form of INJECTION. It is approved for INTRAVENOUS use.
This product is manufactured by FRESENIUS KABI AB in SWEDEN.
It is an Over-the-counter Medicine that can be freely obtained from any retailer
Product Reference
Important Note: For generic product, the SPC/PIL provided may not be brand specific.
{{/items}} {{^items}}Description
Retinol and derivatives of retinol that play an essential role in metabolic functioning of the retina, the growth of and differentiation of epithelial tissue, the growth of bone, reproduction, and the immune response. Dietary vitamin A is derived from a variety of carotenoids found in plants. It is enriched in the liver, egg yolks, and the fat component of dairy products. [PubChem]
Indication
For the treatment of vitamin A deficiency.
Mechanism of Action
Vision:Vitamin A (all-trans retinol) is converted in the retina to the 11-cis-isomer of retinaldehyde or 11-cis-retinal. 11-cis-retinal functions in the retina in the transduction of light into the neural signals necessary for vision. 11-cis-retinal, while attached to opsin in rhodopsin is isomerized to all-trans-retinal by light. This is the event that triggers the nerve impulse to the brain which allows for the perception of light. All-trans-retinal is then released from opsin and reduced to all-trans-retinol. All-trans-retinol is isomerized to 11-cis-retinol in the dark, and then oxidized to 11-cis-retinal. 11-cis-retinal recombines with opsin to re-form rhodopsin. Night blindness or defective vision at low illumination results from a failure to re-synthesize 11-cis retinal rapidly.
Epithelial differentiation: The role of Vitamin A in epithelial differentiation, as well as in other physiological processes, involves the binding of Vitamin A to two families of nuclear retinoid receptors (retinoic acid receptors, RARs; and retinoid-X receptors, RXRs). These receptors function as ligand-activated transcription factors that modulate gene transcription. When there is not enough Vitamin A to bind these receptors, natural cell differentiation and growth are interrupted.
Pharmacokinetics
- Absorption
- Readily absorbed from the normal gastrointestinal tract
- Distribution
- Metabolism
- Hepatic. Retinol is conjugated with glucuronic acid; the B-glucuronide undergoes enterohepatic circulation and oxidation to retinol and retinoic acid. Retinoic acid undergoes decarboxylation and conjugation with glucuronic acid.
- Elimination
Toxicity
Acute toxicity (single ingestion of 7 500 RE or 25 000 IU per kg or more): Signs and symptoms may be delayed for 8 to 24 hours and include: increased intracranial pressure, headache, irritability, drowsiness, dizziness, lethargy, vomiting, diarrhea, bulging of fontanels in infants, diplopia, papilledema. Peeling of skin around mouth may be observed from 1 to several days after ingestion and may spread to the rest of the body. Chronic, excessive ingestion (1 200 RE or 4 000 IU/kg daily for 6 to 15 months) may produce symptoms of pseudotumor cerebri, anorexia, weakness, arthralgias, bone pain, bone demineralization, dry skin, cracked lips, brittle nails, hair loss, splenomegaly, hepatomegaly, hypoplastic anemia, leukopenia, optic neuropathy, and blindness. Increased plasma concentrations of vitamin A occur but do not necessarily correlate with toxicity.
Active Ingredient/Synonyms
(2E,4E,6E,8E)-3,7-dimethyl-9-(2,6,6-trimethylcyclohex-1-en-1-yl)nona-2,4,6,8-tetraen-1-ol | all-trans-retinol | all-trans-retinyl alcohol | all-trans-vitamin A alcohol | Retinol | Vitamin A1 | Vitamin A |
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
Ergocalciferol (Vitamin D2) is a derivative of ergosterol formed by ultraviolet rays breaking of the C9-C10 bond. It differs from cholecalciferol in having a double bond between C22 and C23 and a methyl group at C24.
Indication
For use in the management of hypocalcemia and its clinical manifestations in patients with hypoparathyroidism, as well as for the treatment of familial hypophosphatemia (vitamin D resistant rickets). This drug has also been used in the treatment of nutritional rickets or osteomalacia, vitamin D dependent rickets, rickets or osteomalacia secondary to long-term high dose anticonvulsant therapy, early renal osteodystrophy, osteoporosis (in conjunction with calcium), and hypophosphatemia associated with Fanconi syndrome (with treatment of acidosis).
Mechanism of Action
Activated ergocalciferol increases serum calcium and phosphate concentrations, primarily by increasing intestinal absorption of calcium and phosphate through binding to a specific receptor in the mucosal cytoplasm of the intestine. Subsequently, calcium is absorbed through formation of a calcium-binding protein. 25-hydroxyergocalciferol is the intermediary metabolite of ergocalciferol. Although this metabolite exhibits 2–5 times more activity than unactivated ergocalciferol in curing rickets and inducing calcium absorption and mobilization (from bone) in animals, this increased activity is still insufficient to affect these functions at physiologic concentrations. Activated ergocalciferol stimulate resorption of bone and are required for normal mineralization of bone. Physiological doses of ergocalciferol also promotes calcium reabsorption by the kidneys, but the significance of this effect is not known.
Pharmacokinetics
- Absorption
- Readily absorbed from small intestine (proximal or distal), requires presence of bile salts.
- Distribution
- Metabolism
- Within the liver, ergocalciferol is hydroxylated to ercalcidiol (25-hydroxyergocalciferol) by the enzyme 25-hydroxylase. Within the kidney, ercalcidiol serves as a substrate for 1-alpha-hydroxylase, yielding ercalcitriol (1,25-dihydroxyergocalciferol), the biologically active form of vitamin D2.
- Elimination
Toxicity
LD50 = 23.7 mg/kg (Orally in mice); LD50 = 10 mg/kg (Orally in rats ); Nausea, vomiting and diarrhea, weight loss, irritability, weakness, fatigue, lassitude, and headache.
Active Ingredient/Synonyms
(3β,5Z,7E,22E)-9,10-secoergosta-5,7,10(19),22-tetraen-3-ol | (5Z,7E,22E)-(3S)-9,10-seco-5,7,10(19),22-ergostatetraen-3-ol | (5Z,7E,22E)-(3S)-9,10-secoergosta-5,7,10(19),22-tetraen-3-ol | Activated ergosterol | Ercalciol | Ergocalciférol | Ergocalciferol | Ergocalciferolum | Oleovitamin D2 | Viosterol | Vitamin D2 | Vitamina D2 | Ergocalciferol |
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 generic descriptor for all tocopherols and tocotrienols that exhibit alpha-tocopherol activity. By virtue of the phenolic hydrogen on the 2H-1-benzopyran-6-ol nucleus, these compounds exhibit varying degree of antioxidant activity, depending on the site and number of methyl groups and the type of isoprenoids.
Indication
Vitamin E, known for its antioxidant activities, is protective against cardiovascular disease and some forms of cancer and has also demonstrated immune-enhancing effects. It may be of limited benefit in some with asthma and rheumatoid arthritis. It may be helpful in some neurological diseases including Alzheimer's, some eye disorders including cataracts, and diabetes and premenstrual syndrome. It may also help protect skin from ultraviolet irradiation although claims that it reverses skin aging, enhances male fertility and exercise performance are poorly supported. It may help relieve some muscle cramps.
Mechanism of Action
Although all forms of Vitamin E exhibit antioxidant activity, it is known that the antioxidant activity of vitamin E is not sufficient to explain the vitamin's biological activity.
Vitamin E's anti-atherogenic activity involves the inhibition of the oxidation of LDL and the accumulation of oxLDL in the arterial wall. It also appears to reduce oxLDL-induced apoptosis in human endothelial cells. Oxidation of LDL is a key early step in atherogenesis as it triggers a number of events which lead to the formation of atherosclerotic plaque. In addition, vitamin E inhibits protein kinase C (PKC) activity. PKC plays a role in smooth muscle cell proliferation, and, thus, the inhibition of PKC results in inhibition of smooth muscle cell proliferation, which is involved in atherogenesis.
Vitamin E's antithrombotic and anticoagulant activities involves the downregulation of the expression of intracellular cell adhesion molecule(ICAM)-1 and vascular cell adhesion molecule(VCAM)-1 which lowers the adhesion of blood components to the endothelium. In addition, vitamin E upregulates the expression of cytosolic phospholipase A2 and cyclooxygenase (COX)-1 which in turn enhances the release of prostacyclin. Prostacyclin is a vasodilating factor and inhibitor of platelet aggregation and platelet release. It is also known that platelet aggregation is mediated by a mechanism involving the binding of fibrinogen to the glycoprotein IIb/IIIa (GPIIb/IIIa) complex of platelets. GPIIb/IIIa is the major membrane receptor protein that is key to the role of the platelet aggregation response. GPIIb is the alpha-subunit of this platelet membrane protein. Alpha-tocopherol downregulates GPIIb promoter activity which results in reduction of GPIIb protein expression and decreased platelet aggregation. Vitamin E has also been found in culture to decrease plasma production of thrombin, a protein which binds to platelets and induces aggregation. A metabolite of vitamin E called vitamin E quinone or alpha-tocopheryl quinone (TQ) is a potent anticoagulant. This metabolite inhibits vitamin K-dependent carboxylase, which is a major enzyme in the coagulation cascade.
The neuroprotective effects of vitamin E are explained by its antioxidant effects. Many disorders of the nervous system are caused by oxidative stress. Vitamin E protects against this stress, thereby protecting the nervouse system.
The immunomodulatory effects of Vitamin E have been demonstrated in vitro, where alpha-tocopherol increases mitogenic response of T lymphocytes from aged mice. The mechanism of this response by vitamin E is not well understood, however it has been suggested that vitamin E itself may have mitogenic activity independent of its antioxidant activity.
Lastly, the mechanism of action of vitamin E's antiviral effects (primarily against HIV-1) involves its antioxidant activity. Vitamin E reduces oxidative stress, which is thought to contribute to HIV-1 pathogenesis, as well as to the pathogenesis of other viral infections. Vitamin E also affects membrane integrity and fluidity and, since HIV-1 is a membraned virus, altering membrane fluidity of HIV-1 may interfere with its ability to bind to cell-receptor sites, thus decreasing its infectivity.
Pharmacokinetics
- Absorption
- 50 to 80% absorbed from gastrointestinal tract.
- Distribution
- Metabolism
- Hepatic.
- Elimination
Active Ingredient/Synonyms
(+)-α-tocopherol | (2R,4'R,8'R)-α-tocopherol | (2R)-2,5,7,8-TETRAMETHYL-2-[(4R,8R)-4,8,12-TRIMETHYLTRIDECYL]CHROMAN-6-OL | (R,R,R)-α-tocopherol | 5,7,8-trimethyltocol | alpha-tocopherol | d-α-tocopherol | Vitamin E |
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
Phylloquinone is often called vitamin K1. It is a fat-soluble vitamin that is stable to air and moisture but decomposes in sunlight. It is found naturally in a wide variety of green plants. Phylloquinone is also an antidote for coumatetralyl. Vitamin K is needed for the posttranslational modification of certain proteins, mostly required for blood coagulation.
Indication
For the treatment of haemorrhagic conditions in infants, antidote for coumarin anticoagulants in hypoprothrombinaemia.
Mechanism of Action
Vitamin K is an essential cofactor for the gamma-carboxylase enzymes which catalyze the posttranslational gamma-carboxylation of glutamic acid residues in inactive hepatic precursors of coagulation factors II (prothrombin), VII, IX and X. Gamma-carboxylation converts these inactive precursors into active coagulation factors which are secreted by hepatocytes into the blood. Supplementing with Phylloquinone results in a relief of vitamin K deficiency symptoms which include easy bruisability, epistaxis, gastrointestinal bleeding, menorrhagia and hematuria.
Pharmacokinetics
- Absorption
- Oral phylloquinone is adequately absorbed from the gastrointestinal tract only if bile salts are present. After absorption, phylloquinone is initially concentrated in the liver, but the concentration declines rapidly. Very little vitamin K accumulates in tissues.
- Distribution
- Metabolism
- Elimination
Toxicity
The intravenous LD50 of phylloquinone in the mouse is 41.5 and 52 mL/kg for the 0.2% and 1% concentrations, respectively.
Active Ingredient/Synonyms
2-Methyl-3-(3,7,11,15-tetramethyl-2-hexadecenyl)-1,4-naphthalenedione | 2-Methyl-3-[(2e)-3,7,11,15-tetramethyl-2-hexadecenyl]naphthoquinone | 2-Methyl-3-phytyl-1,4-naphthochinon | 2-Methyl-3-phytyl-1,4-naphthoquinone | 3-Phytylmenadione | alpha-Phylloquinone | Fitomenadiona | Phyllochinon | Phyllochinonum | Phylloquinone | Phythyl-menadion | Phytomenadione | Phytomenadionum | Phytonadionum | Phytylmenadione | trans-Phylloquinone | Vitamin k | Vitamin K1 | α-phylloquinone | Phylloquinone |
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.