MEBAAL-500 Mecobalamin (Vit. B12) 500mcg Film-Coated Tablet 1's
RXDRUG-DR-XY37578-1pc
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Features
Brand
Mebaal-500
GTIN
8850769018738
Full Details
Dosage Strength
500mcg
Drug Ingredients
- Mecobalamin
Drug Packaging
Film-Coated Tablet 1's
Generic Name
Mecobalamin
Dosage Form
Film-Coated Tablet
Registration Number
DR-XY37578
Drug Classification
Prescription Drug (RX)
Description
Indications/Uses
Peripheral neuropathy, dementia, alcoholic neuropathy, drug-induced neuropathy, trigeminal and occupational neuralgia, Parkinson disease, Bell's palsy, megaloblastic anemia, cancer, male impotence, hyperhomocysteinemia, sleep disturbances.
Dosage/Direction for Use
Take one (1) tablet, once or twice daily, or as recommended by a physician.
Administration
May be taken with or without food.
Special Precautions
The use of mecobalamin in deficiency states or to treat any medical condition requires medical supervision dose as nutritional supplements used by pregnant women and nursing mothers is 12 micrograms daily. Pregnant women and nursing mothers should only use doses higher than this if recommended by the physicians. Administration of doses greater than 10 micrograms daily may produce a hematological response in those with anemia secondary to folate deficiency.
Adverse Reactions
Anaphylactic reaction: Anaphylactic reaction such as decrease in blood pressure or dyspnea may occur. Patient should be monitored after administration of dose.
Drug Interactions
Antibiotics: The use of antibiotics may alter the intestinal microflora and may decrease the possible contribution of mecobalamin by certain inhabitants of the microflora (e.g. Lactobacillus species) to the body's requirement for the vitamin. This may particularly be a problem for vegetarians. Garlic, onions, leeks, bananas, asparagus and artichokes, among other vegetables and fruits, contain inulins which promote the growth of certain colonic bacteria including Lactobacillus species.
Cholestyramine: Cholestyramine may decrease the enterohepatic reabsorption of mecobalamin.
Colchicine: Colchicine may cause decreased absorption of mecobalamin.
Colestipol: Colestipol may decrease the enterohepatic reabsorption of mecobalamin.
H2 Blockers (cimetidine, famotidine, nizatidine, ranitidine): Chronic use of H2 blockers may result to decreased absorption of mecobalamin. They are unlikely to affect the absorption of supplemental B12.
Metformin: Metformin may decrease the absorption of mecobalamin. This possible effect may be reversed with oral calcium supplementation.
Nitrous Oxide: Inhalation of the anesthetic agent nitrous oxide (not to be confused with nitric oxide) can produce a functional deficiency. Nitrous oxide forms a complex with cobalt in mecobalamin, the cofactor for methionine synthase, resulting in inactivation of the enzyme.
Para-amino Salicylic Acid: Chronic use of the anti-tuberculosis drug may decrease the absorption of mecobalamin.
Potassium chloride: It has been reported that potassium chloride may decrease the absorption of mecobalamin.
Proton Pump Inhibitors (lansoprazole, omeprazole, pantoprazole, rabeprazole): Chronic use of proton pump inhibitors may result in decreased absorption, naturally found in food sources.
Cholestyramine: Cholestyramine may decrease the enterohepatic reabsorption of mecobalamin.
Colchicine: Colchicine may cause decreased absorption of mecobalamin.
Colestipol: Colestipol may decrease the enterohepatic reabsorption of mecobalamin.
H2 Blockers (cimetidine, famotidine, nizatidine, ranitidine): Chronic use of H2 blockers may result to decreased absorption of mecobalamin. They are unlikely to affect the absorption of supplemental B12.
Metformin: Metformin may decrease the absorption of mecobalamin. This possible effect may be reversed with oral calcium supplementation.
Nitrous Oxide: Inhalation of the anesthetic agent nitrous oxide (not to be confused with nitric oxide) can produce a functional deficiency. Nitrous oxide forms a complex with cobalt in mecobalamin, the cofactor for methionine synthase, resulting in inactivation of the enzyme.
Para-amino Salicylic Acid: Chronic use of the anti-tuberculosis drug may decrease the absorption of mecobalamin.
Potassium chloride: It has been reported that potassium chloride may decrease the absorption of mecobalamin.
Proton Pump Inhibitors (lansoprazole, omeprazole, pantoprazole, rabeprazole): Chronic use of proton pump inhibitors may result in decreased absorption, naturally found in food sources.
Storage
Store at temperatures not exceeding 30°C.
Action
Pharmacology: Mecobalamin plays an important role in transmethylation as a coenzyme of methionine synthesis from homocysteine.
Mecobalamin is well transported to nerve cell organelles and promotes nucleic acid and protein synthesis. It is better transported to nerve cell organelles than cyanocobalamin in animals.
Mecobalamin promotes axonal regeneration. It normalizes axonal skeletal protein transport in sciatic nerve cells from animal models with streptozotocin-induced diabetes mellitus. It exhibits neuropathologically and electrophysiologically inhibitory effects on nerve degeneration in neuropathies induced by drugs eg, adriamycin, acrylamide and vincristine models of axonal degeneration in mice and neuropathies in animals with spontaneous diabetes mellitus.
Mecobalamin promotes myelination (phospholipid synthesis). It promotes the synthesis of lecithin, the main constituent of medullary sheath lipid and increases myelination of neuron in animal tissue culture more than cobalamide does.
Mecobalamin restores delayed synaptic transmission and diminished neurotransmitters to normal. It restores end-plate potential induction early by increasing fiber excitability in crushed sciatic nerve. In addition, it also normalizes diminished brain tissue levels of acetylcholine in animals fed with a choline-deficient diet.
Mecobalamin promotes the maturation and division of erythroblasts, thereby alleviating anemia. It also promotes nucleic acid synthesis in bone marrow and the maturation and division of erythroblasts, thereby increasing erythrocyte production.
Mecobalamin brings about a rapid recovery of diminished red blood cell and hematocrit in vitamin B-12 deficient animals.
Pharmacokinetics: Naturally found B12 is dissociated from proteins in the stomach via the action of acid and the enzyme pepsin. The forms of B12 released by this process are Mecobalamin (methylcobalamin) and adenosylcobalamin. All forms of B12 bind to proteins called haptocorrins or R proteins, which are secreted by the salivary glands and the gastric mucosa. This binding occurs in the stomach. Pancreatic proteases partially degrade the cobalamin-haptocorrin complexes in the small intestine where cobalamin that is released then binds to intrinsic factor (IF). Intrinsic factor is a glycoprotein which is secreted by gastric parietal cells. The cobalamin-intrinsic factor complex is absorbed from the terminal ileum into the ileal enterocytes, cobalamin is released from the cobalamin-IF complex and then binds to another protein called transcobalamin II that delivers it to the portal circulation. The portal circulation transports cobalamin to the liver which takes up about 50% of the vitamin; the reminder is transported to the other tissues of the body via the systemic circulation. The cobalamin-transcobalamin II complex is degraded intracellularly via lysosomal proteases to yield cobalamin (cyanocobalamin, mecobalamin, adenosylcobalamin, hydroxocobalamin). Cobalamin is metabolized to mecobalamin in the cytosol and to adenosylcobalamin in the mitochondria. Mecobalamin is the principal circulating form of cobalamin. Adenosylcobalamin comprises more than 70% of cobalamin in the liver, erythrocytes, kidney and brain. The total body content of cobalamin ranges from 2-3 mg, with approximately 50% of it residing in the liver.
Mecobalamin in the circulation is bound to the plasma proteins transcobalamin I (TCI), transcobalamin II (TCII) and transcobalamin III (TCIII). Approximately 80% of plasma B12 is bound to TCI. TCII is the principal B12 binding protein for the delivery of B12 to cells via specific receptors for TCII. This B12 binding protein (TCII) is identical to the one that delivers B12 from the enterocytes to the portal circulation.
Total absorption increases with increased intake of vitamin. However, the absorption efficacy of the vitamin decreases with increased dosage. Significantly, very large doses of mecobalamin are absorbed in the absence of intrinsic factor. Thus, large oral doses may be given for the treatment of deficiency instead of using the parenteral route (usually intramuscularly). There are now several studies confirming this. The absorption efficiency of mecobalamin from food is approximately 50%.
Mecobalamin is secreted in the bile and reabsorbed via the enterohepatic circulation. Some of them, which are secreted in the bile, are excreted in the feces. Also, oral B12 that is not absorbed is excreted in the feces. Reabsorption of mecobalamin via the enterohepatic circulation does not require the intrinsic factor. If the circulating level of B12 exceeds the B12 binding capacity of the blood, a situation that usually occurs following parenteral administration of the vitamin, the excess is excreted in the urine.
Blood levels of patients indicate that the sublingual mecobalamin becomes available as early as 15 min after administration and is still elevated at 24 hours. It is absorbed through the oral mucosa, which bypasses the need for it to bind with intrinsic factor in the stomach. Eighty percent (80%) of B12 in the plasma is the mecobalamin form.
Mecobalamin is well transported to nerve cell organelles and promotes nucleic acid and protein synthesis. It is better transported to nerve cell organelles than cyanocobalamin in animals.
Mecobalamin promotes axonal regeneration. It normalizes axonal skeletal protein transport in sciatic nerve cells from animal models with streptozotocin-induced diabetes mellitus. It exhibits neuropathologically and electrophysiologically inhibitory effects on nerve degeneration in neuropathies induced by drugs eg, adriamycin, acrylamide and vincristine models of axonal degeneration in mice and neuropathies in animals with spontaneous diabetes mellitus.
Mecobalamin promotes myelination (phospholipid synthesis). It promotes the synthesis of lecithin, the main constituent of medullary sheath lipid and increases myelination of neuron in animal tissue culture more than cobalamide does.
Mecobalamin restores delayed synaptic transmission and diminished neurotransmitters to normal. It restores end-plate potential induction early by increasing fiber excitability in crushed sciatic nerve. In addition, it also normalizes diminished brain tissue levels of acetylcholine in animals fed with a choline-deficient diet.
Mecobalamin promotes the maturation and division of erythroblasts, thereby alleviating anemia. It also promotes nucleic acid synthesis in bone marrow and the maturation and division of erythroblasts, thereby increasing erythrocyte production.
Mecobalamin brings about a rapid recovery of diminished red blood cell and hematocrit in vitamin B-12 deficient animals.
Pharmacokinetics: Naturally found B12 is dissociated from proteins in the stomach via the action of acid and the enzyme pepsin. The forms of B12 released by this process are Mecobalamin (methylcobalamin) and adenosylcobalamin. All forms of B12 bind to proteins called haptocorrins or R proteins, which are secreted by the salivary glands and the gastric mucosa. This binding occurs in the stomach. Pancreatic proteases partially degrade the cobalamin-haptocorrin complexes in the small intestine where cobalamin that is released then binds to intrinsic factor (IF). Intrinsic factor is a glycoprotein which is secreted by gastric parietal cells. The cobalamin-intrinsic factor complex is absorbed from the terminal ileum into the ileal enterocytes, cobalamin is released from the cobalamin-IF complex and then binds to another protein called transcobalamin II that delivers it to the portal circulation. The portal circulation transports cobalamin to the liver which takes up about 50% of the vitamin; the reminder is transported to the other tissues of the body via the systemic circulation. The cobalamin-transcobalamin II complex is degraded intracellularly via lysosomal proteases to yield cobalamin (cyanocobalamin, mecobalamin, adenosylcobalamin, hydroxocobalamin). Cobalamin is metabolized to mecobalamin in the cytosol and to adenosylcobalamin in the mitochondria. Mecobalamin is the principal circulating form of cobalamin. Adenosylcobalamin comprises more than 70% of cobalamin in the liver, erythrocytes, kidney and brain. The total body content of cobalamin ranges from 2-3 mg, with approximately 50% of it residing in the liver.
Mecobalamin in the circulation is bound to the plasma proteins transcobalamin I (TCI), transcobalamin II (TCII) and transcobalamin III (TCIII). Approximately 80% of plasma B12 is bound to TCI. TCII is the principal B12 binding protein for the delivery of B12 to cells via specific receptors for TCII. This B12 binding protein (TCII) is identical to the one that delivers B12 from the enterocytes to the portal circulation.
Total absorption increases with increased intake of vitamin. However, the absorption efficacy of the vitamin decreases with increased dosage. Significantly, very large doses of mecobalamin are absorbed in the absence of intrinsic factor. Thus, large oral doses may be given for the treatment of deficiency instead of using the parenteral route (usually intramuscularly). There are now several studies confirming this. The absorption efficiency of mecobalamin from food is approximately 50%.
Mecobalamin is secreted in the bile and reabsorbed via the enterohepatic circulation. Some of them, which are secreted in the bile, are excreted in the feces. Also, oral B12 that is not absorbed is excreted in the feces. Reabsorption of mecobalamin via the enterohepatic circulation does not require the intrinsic factor. If the circulating level of B12 exceeds the B12 binding capacity of the blood, a situation that usually occurs following parenteral administration of the vitamin, the excess is excreted in the urine.
Blood levels of patients indicate that the sublingual mecobalamin becomes available as early as 15 min after administration and is still elevated at 24 hours. It is absorbed through the oral mucosa, which bypasses the need for it to bind with intrinsic factor in the stomach. Eighty percent (80%) of B12 in the plasma is the mecobalamin form.
MedsGo Class
Nootropics & Neurotonics/Neurotrophics
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