But they already have a compound for parks, don't they?
What Are The Treatment Options For Parkinson’s Disease? Click For Info
Medication Medication - as most Parkinson’s symptoms are caused by low levels of dopamine in the brain, most drugs are aimed at either replenishing dopamine levels, or mimicking its action - dopaminergic drugs do this. Dopaminergic medications reduce rigidity (muscle stiffness), improve speed, help with coordination, and lessen tremor (shaking). Taking dopamine itself does not help, because it cannot enter the brain.
Levodopa - the most effective Parkinson’s drug; is absorbed by the nerve cells in the brain and turned into dopamine. It is taken orally, in tablet or liquid form. Levodopa is combined with carbidopa to create Sinemet, a combination drug. Carbidopa prevents the levodopa from being destroyed by enzymes in the digestive tract; it also reduces levodopa side effects, such as nausea, vomiting, fatigue and dizziness. In the UK and the rest of Europe benserazide may be combined with levodopa (Madopar).
As Parkinson’s disease progresses the effects of levodopa may wear off and the doctor may have to increase the dosage. Increased dosage also raises the risk of developing side effects, which may include confusion, delusions, hallucinations, compulsive behavior, and dyskinesia (involuntary movements). Reducing the dosage will usually help with side effects, but with the risk that parkinsonism increases.
Dopamine agonists - these drugs mimic the effects of dopamine in the brain. The neurons react as they would to dopamine. Although not as effective as levodopa, dopamine agonists last longer and help reduce the waning effect of levodopa. They are usually prescribed in tablet form, but may also be taken by injection, or as a skin-patch. Examples include pramipexole (Mirapex), ropinirole (Requip), rotigotine (Neupro), and apomorphine (Apokyn).
Side effects are similar to those of carbidopa-levodopa. The risk of developing compulsive behaviors, such as compulsive gambling and hypersexuality are greater. Monoamine oxidase-B inhibitors (MAO B inhibitors) - an alternative to levodopa. Examples include selegiline and rasagiline. MAO B inhibitors work by blocking the effects of monoamine oxidase-B (MAO B) in the brain. Monoamine oxidase-B destroys dopamine - by blocking MAO B the dopamine can last longer in the brain. MAO B inhibitors have a smaller effect than levodopa. MAO B inhibitors can be used in combination with levodopa or dopamine agonists. There is a risk of serious interactions with some medications used for treating depression, as well as some narcotics.
Side effects of selegiline may include: Dizziness Dry mouth Headaches Nausea Stomach pain Strange and/or vivid dreams
Side effects of rasagiline may include: Conjunctivitis Dizziness Fever, with joint and muscle aches (flu-like) Headache Indigestion Neck pain Runny nose Stomach pain
COMT (catechol O-methyltransferase) inhibitors - this medication blocks the enzyme that breaks down levodopa, hence prolonging the effect of carbidopa-levodopa therapy. Anticholinergics - used for controlling tremor (shaking). Examples include trihexyphenidyl and benztropine (Cogentin). Some patients may find that the side effects are much greater than the slight benefits. Side effects may include urine retention, severe constipation, nausea and dry mouth. Male patients with an enlarged prostate have a higher risk of developing urine retention. Antivirals - may be used on its own during early-stage Parkinson’s disease. May also be used alongside carbidopa-levodopa therapy later on. Side effects include ankle edema (swelling) and skin discoloration. An example of this drug is amantadine (Symmetrel).
It is used in the management of Parkinson's disease in combination with L-DOPA (levodopa) as co-beneldopa (BAN), under the brand names Madopar in the UK and Prolopa in Canada, both made by Roche. Benserazide is not approved for use in the US; carbidopa is used instead for the same purpose. These combinations are also used for the treatment of restless legs syndrome.[2]
Pharmacology[edit] Levodopa is a precursor to the neurotransmitter dopamine which is administered to increase its levels in the central nervous system. However, most levodopa is decarboxylated to dopamine before it reaches the brain, and since dopamine is unable to cross the blood–brain barrier, this translates to little therapeutic gain with strong peripheral side effects.
Benserazide inhibits the aforementioned decarboxylation, and since it itself cannot cross the blood–brain barrier, this allows dopamine to build up solely in the brain instead. Adverse effects caused by peripheral dopamine, such as vasoconstriction, nausea, and arrhythmia, are minimized. However, benserazide cannot reduce the centrally-mediated side effects of levodopa, particularly dyskinesia.
Benserazide has little therapeutic effect on its own, and it's effect occurs synergically in combination with levodopa.
The enzyme inhibited by Benzerazide, catalyzes many different decarboxylations. The same effect of concentrating the conversion of l-dopa into dopamine to the central nervous system can be achieved with the following decarboxylations being confined to the central nervous system:
5-htp to serotonin Tryptophan to Tryptamine Phenylalanine to Phenethylamine L-Tyrosine to Tyramine Centrally-mediated side effects of higher levels of neuro and trace amine transmitters may worsen in combination with monoamine oxidase inhibitors.
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