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Top Purity Nootropic Supplements Rivastigmine Tartrate CAS 129101-54-8

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Top Purity Nootropic Supplements Rivastigmine Tartrate CAS 129101-54-8

Top Purity Nootropic Supplements Rivastigmine Tartrate CAS 129101-54-8
Top Purity Nootropic Supplements Rivastigmine Tartrate CAS 129101-54-8

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Product Details:

Place of Origin: China
Brand Name: SGH
Certification: GMP, ISO9001,BRC,KOSHER
Model Number: 129101-54-8

Payment & Shipping Terms:

Minimum Order Quantity: 10g
Price: Negotiation
Packaging Details: Discreet package or foiled bag or pack as customer's request
Payment Terms: T/T, Western Union, MoneyGram, Bitcoin
Supply Ability: 100kg/Month
Detailed Product Description
CAS NO: 129101-54-8 Synonyms: Rivastigmine
Form: Powder Usage: Loss Weight
Color: White Storage: -20C
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Top Purity Nootropic Supplements Rivastigmine Tartrate CAS 129101-54-8

 

Description:

 

Rivastigmine (sold under the trade name Exelon) is a parasympathomimetic or cholinergic agent for the treatment of mild to moderate dementia of the Alzheimer's type and dementia due to Parkinson's disease. The drug can be administered orally or via a transdermal patch; the latter form reduces the prevalence of side effects, which typically include nausea and vomiting.

 

Rivastigmine Tartrate is rivastigmine Alzheimer's disease drugs, rivastigmine is physostigmine derivative by Novartis for the first time successfully developed the trade name Exelon (exelon), a molecule with there carbamate structure, is a kind of amino acid of selective cerebral cholinesterase inhibitor, can also inhibit the acetylcholinesterase and butyrylcholinesterase, cholinergic neurons by delaying the release of acetylcholine degradation and energy promoting cholinergic nerve conduction, can improve cognitive function disorders mediated by cholinergic, thereby improving the cognitive function of Alzheimer's disease patients.

 

 

Application:

 

Rivastigmine improves the function of nerve cells in the brain. It works by preventing the breakdown of a chemical that is important for the processes of memory, thinking, and reasoning. People with dementia usually have lower levels of this chemical.
Rivastigmine is used to treat mild to moderate dementia caused by Alzheimer's or Parkinson's disease.
Rivastigmine may also be used for purposes not listed in this medication guide.
Rivastigmine Tartrate plasma protein binding is weak, easily through the blood-brain barrier, which has a high degree of brain selectivity. It not only selectively acts on the most easily affected cerebral cortex and hippocampus, but also preferentially inhibits the dominant subtype of AChE in the brain, resulting in a reduction in the efficacy of peripheral cholinergic side effects. Rivastigmine in vivo half-life is short and long duration of action. Unlike tacrine, this product in the hippocampus and cortex of G1 enzyme inhibitory effect is stronger. Clinic for the treatment of mild to moderate Alzheimer-type dementia, or Alzheimer's disease can be suspected Alzheimer's disease clinically.

Pathological changes in Alzheimer's disease mainly involve the cholinergic nerve pathways from the basal forebrain to the cerebral cortex and hippocampus. These pathways are known to be related to attention, learning ability, memory, and other cognitive processes.
Carbamate tartrate is a carbamate-selective acetylcholinesterase inhibitor that promotes cholinergic nerve conduction by delaying the function of complete cholinergic neurons to release the release of acetylcholine. The results of animal experiments showed that valacridine tartrate could selectively enhance the effect of acetylcholine in cerebral cortex and hippocampus.
Therefore, Aisi can improve Alzheimer's disease in patients with cholinergic-mediated cognitive dysfunction. In addition, cholinesterase inhibitors can slow the formation of amyloid b-amyloid precursor protein (APP) fragments. Amyloid plaque is Alzheimer's disease tartaric acid rivastigmine by the target enzyme into a covalent complex and the latter temporarily lost activity.

The activity of acetylcholinesterase in cerebrospinal fluid (CSF) decreased by nearly 40% within 1.5 hours after 3 mg of human administration. After the drug reaches its maximum inhibitory effect, the enzyme activity is restored to the basal level for approximately 9 hours. The inhibition of acetylcholinesterase in ruthenate tartrate in patients with Alzheimer's disease was dose-dependent, with a maximum test dose of 6 mg twice daily.

 

 

 

 

 

 

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