Pharmacodynamics

Mechanism of Action

1) Mecobalamin is a kind of endogenous coenzyme B12

Mecobalamin plays an important role in transmethylation as a coenzyme of methionine synthetase in the synthesis of methionine from homocysteine.

2) Mecobalamin is well transported to nerve cell organelles and promotes nucleic acid and protein synthesis.

Mecobalamin is better transported to nerve cell organelles than cyanocobalamin in rats. It has been shown in experiments with cells from the brain origin and spinal nerve cells in rats to be

involved in the synthesis of thymidine from deoxyuridine, promotion of deposited folic acid utilization and metabolism of nucleic acid. AJso, mecobalamin promotes nucleic acid and protein synthesis in rats more than cobamamide does.

3) Mecobalamin promotes axonal transport and axonal regeneration.

Mecobalamin normalizes axonal skeletal protein transport in sciatic nerve cells from rat models with streptozotocin-induced diabetes mellitus. It exhibits neuropathologically and electrophysiologically inhibitory effects on nerve degeneration neuropathies induced by drugs, such as Adriamycin, acrylamide, and vincristine (in rats and rabbits), models of axonal degeneration in mice and neuropathies such as adriamycin, acrylamide, and vincristine (in rats and rabbits), models of axonal degeneration in mice and neuropathies in rats with spontaneous diabetes mellitus.

4) Mecobalamin promotes myelination (phospholipid synthesis)

Mecobalamin promotes the synthesis of lecithin, the main constituent of medullary sheath lipid and increases myelination of neurons in rat tissue culture more than cobamamide does.

5) Mecobalamin restores delayed synaptic transmission and diminished neurotransmitters to normal.

Mecobalamin restores end-plate potential induction early by increasing nerve fiber excitability in the crushed sciatic nerve in rats. In addition, mecobalamin normalizes diminished brain tissue levels of acetylcholine in rats fed a choline-deficient diet.

6) Mecobalamin promotes the maturation and division of erythroblasts, thereby alleviating anemia.

It is well known that vitamin B12-deficiency may cause specific megaloblastic anemia. Mecobalamin promotes nucleic acid synthesis in bone marrow and promotes the maturation and division of erythroblasts, thereby increasing erythrocyte production. Mecobalamin brigs about a rapid recovery of diminished red blood cell, hemoglobin, and hematocrit in vitamin B12-deficienct rats.


Clinical Studies

Clinical efficacy

Mecobalamin was administered intramuscularly to patients with peripheral neuropathies in single doses of 500 mcg and 100 mcg (low-dose group) daily 3 times a week for 4 consecutive weeks in a double-blind clinical trial. In the chronic stage and fixed stage of peripheral neuropathies in the 500 mcg group aggravation of symptoms was significantly suppressed compared to the low-dose group and this dose was thus demonstrated to be useful.

ln a placebo-controlled double-blind clinical trial, mecobalamin was administered intravenously or intramuscularly to patients with peripheral neuropathies at a single dose of 500 mcg daily 3 times a week for 4 consecutive weeks. The improvement rate for intravenous administration was 38.7%  (24/62) for moderately to remarkably improved and 74.2% (46/62) for fairly to remarkably improved. The improvement rate for intramuscular administration was 46.3% (25/54) for moderately to remarkably improved and 81.5% (44.54) for fairly to remarkably improved.

The equivalence of mecobalamin efficacy for both administration routes was thus demonstrated. The diseases of subjects in the trial were diabetic neuropathy, polyneuritis, cervical spondylosis, sciatica, alcoholic neuropathy, facial paralysis and mononeuritis, etc.

When mecobalamin was administered to patients with megaloblastic anemia due to vitamin B12  deficiency, their hemograms and symptoms improved in 3 weeks to 2 months after starting administration.