Monosialotetrahexosyl ganglioside Sodium(GM1) powder (Pig Brain) (37758-47-7)

Monosialotetrahexosylganglioside Sodium (GM1) powder pig brain extracted from pig brain. Useful as an antigen and receptor for cholera toxin, as a growthinhibition marker in fibroblasts, and as a marker for lymphoid subpopulations.Monosialotetrahexosylganglioside Sodium powder, one of the glycosphingolipids widely distributed in all tissues, occurs in highest concentrations in the central nervous system. It is primarily located in the outer surface of the mammalian cell’s plasma membrane and in synaptic membranes of the CNS. Monosialotetrahexosylganglioside Sodium modulates a number of cell surface and receptor activities as well as neuronal differentiation and development, protein phosphorylation and synaptic function. In addition, it exerts anti-excitotoxic activity, prevents necrosis, and improves neuronal recovery and function. Check for active clinical trials using this agent.

The study of GM1 powder and its role in neuroprotection dates back to 1970s. Since then, research scientists have shown interest in the compound by carrying out cell cultures and animal studies. All the experiments focused on establishing the significance of GM1 in neurodegenerative disorders.

In 1986, through TRB S.A, Monosialotetrahexosylganglioside sodium was officially launched under the trade name, GM-1. Given that the results on animal studies were promising, the US clinicians set out to investigate Monosialotetrahexosylganglioside sodium (GM1) effects on human. The subjects of the study were patients with CNS damage due to injury of the spinal cord, stroke, Parkinson’s disease, and Alzheimer.

Since then, states such as Argentina and Italy have approved its therapeutic application as a prescription drug for the treatment of neurological conditions.

Monosialotetrahexosyl ganglioside powder works in several ways. The molecule is an epicenter of most of the physiological activities of the nervous system.

In the cell membrane of the brain, Monosialotetrahexosylganglioside functions to maintain the ion balance within and outside the membranous tissue. Not only does it enhance impermeability, but it also evens out sodium and calcium ions pump.

In the case of nerve injury, Monosialotetrahexosylganglioside sodium (GM1) powder comes in to protect the membranous structure. It trims down the activity of phospholipase A2, moderates the calcium ion influx, and cuts down the formation of free radicals.

Brain traumas amplify the activity of protein kinase in the cells, which may be responsible for apoptosis. GM1 inhibits and reverses this process by holding the metabolism of proteins within the cytoplasm and nucleus.

Within the mitochondrion, Monosialotetrahexosylganglioside works to upregulate the production of ATP and its synthase activity. It repairs possible damages on the electron transport chain and improves the oxidative phosphorylation. As a result, the brain’s mitochondrial respiratory function remains healthy.

Monosialotetrahexosylganglioside sodium injection stimulates axonal sprouting by concentrating the growth factors to their specific receptors. This activity regenerates the nerve fibers and promotes rapid neurological recovery. In the case of secondary degeneration, probably due to dopamine neuron damage, Monosialotetrahexosylganglioside will stabilize the effect and enhance the survival of these neurons.

Ganglioside GM1 Sodium Salt (pig brain) is a Specific receptors for cholera toxin that accumulate in the brain in late infantile lipidosis.

Therapeutic applications

Because of GM1’s close role in neurotrophic repair mechanisms, it has been investigated as a potential method to potentially slow or even reverse the progression of a wide range of neurodegenerative conditions. Controlled phase II studies have indicated that GM1 can ease the symptoms of Parkinson’s disease, presumably by countering degeneration of the substantia nigra, and a similar methodology has been pursued to try and limit cellular damage from necrosis and apoptosis occurring after acute spinal cord injury.

COA

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