Pharmacology: Capsule: Biochemically Mecobalamin is a coenzyme form of vitamin B12 with an active methyl group. It participates in transmethylation reactions and is the most active of all B12 homologues in the body with respect to nucleic acid, protein and lipid metabolism. It has also been demonstrated that Mecobalamin facilitates myelogenesis and nerve regeneration. Double-blind clinical trials showed that Mecobalamin is convincingly effective on peripheral neuropathies such as diabetic neurological disorders and multiple neuritis.
Drug Action: Mecobalamin is a homologue of vitamin B12 which participates in transmethylation reactions and plays an important role in the synthesis of nucleic acid and protein in nerve cells. Mecobalamin stimulates Schwan cells and thereby facilitating myelogenesis and enhancing protein synthesis.
Injection: Biochemically mecobalamin is a coenzyme form of vitamin B12 with an active methyl group. It participates in transmethylation reactions and is the most active of all B12 homologues in the body with respect to nucleic acid, protein and lipid metabolism. Metifer acts to repair damaged nerve tissue in nerve disorders, such as axonal degeneration and demyelination; and, it is involved in erythroblast maturation, promotion of erythroblast division, and heme synthesis, thus acting to improve the status of the blood in megaloblastic anemia. Double-blind clinical trials showed, that mecobalamin is effective not only on megaloblastic anemia but also on peripheral neuropathies such as diabetic neurological disorders and multiple neuritis.
Pharmacodynamics: Mecobalamin promotes the metabolism of nucleic acids, proteins and lipids. In an experiment using brain-derived cell strains obtained from albino rats, mecobalamin acted as a coenzyme in methionine synthesis. In particular, it was found to be involved in the synthesis of thymidine from deoxyuridine and to accelerate the synthesis of DNA and RNA. In other experiment using glia cells, mecobalamin was found to accelerate the synthesis of lecithin, a major component of the myelin sheath.
Mecobalamin is efficiently transferred to nerve tissues and improves metabolic disorders. Mecobalamin is a CH3-vitamin B12 which is found in high concentrations in blood and cerebrospinal fluid. In an experiment in rats, it was transferred to nerve cell organelles more efficiently than CN-vitamin B12. It also accelerated the synthesis of the major structural component of the axon (protein) in sciatic nerve cells of rats with experimental diabetes and returned the protein transport rate close to normal, resulting in the maintenance of axonal function.
Mecobalamin repairs nerve tissues in experimental nerve injury models. In experiments conducted in rats and rabbits, mecobalamin was neuropathologically and electrophysiologically shown to inhibit the onset of nerve degeneration due to the disturbances caused by adriamycin and vincristine, and streptozotocin-induced diabetes. Mecobalamin was also compared with steroids in term of their effects on the process of nerve regeneration in experimental facial paralysis models prepared by compressing the facial nerve of guinea pigs. Mecobalamin was found to be as effective as steroids for the recovery from paralysis when evaluated based on the winking reflex, induced electromyography and histological evaluation.
Mecobalamin inhibits abnormal excitation transmission by nerve tissues. The anterior and posterior roots of the spinal nerve were separated from the spinal cord of frogs and connected to the sciatic nerve. Electrical stimulation was given to the end of the sciatic nerve in Ringer's solution and the action potentials of the anterior and posterior roots were recorded. 500 μg/ml of DBCC, OH-vitamin B12, CH3-vitamin B12 were dissolved in the Ringer's solution and the inhibition of excitation transmision by these compounds was compared. The inhibition of nervous excitation transmission produced by CH3-vitamin B12 was the strongest.
Pharmacokinetics: Single dose: Blood concentration peaked (22310 pg/ml) 0.9 hr after the I.m. injection of a single dose of 500 μg of mecobalamin to healthy adults. The half-life was 6.3 hrs. The △Cmax for the increase in serum total vitamin B12 concentration was 21430 pg/ml and the △AUC12 was 185.21 hr·μg/ml.
Multiple doses: Patients with peripheral nerve disorders received an i.m. Injection of 500 μg of mecobalamin three times per week for 12 weeks. Blood vitamin B12 concentration had increased about 15-fold in 4 weeks after the start of treatment: it continued to increase thereafter to achieve a 30-fold increase in 12 weeks after the start of treatment.