Product Information
Registration Status: ActiveSINEMET SR TABLET 50/200 is approved to be sold in Singapore with effective from 2014-03-09. It is marketed by MSD PHARMA (SINGAPORE) PTE LTD, with the registration number of SIN14601P.
This product contains Carbidopa 50mg, and Levodopa 200mg in the form of TABLET, EXTENDED-RELEASE. It is approved for ORAL use.
This product is manufactured by Mylan Pharmaceuticals Inc. in UNITED STATES, andPT. Merck Sharp Dohme Pharma Tbk (Primary and Secondary Packager) in INDONESIA REP OF.
It is a Prescription Only Medicine that can only be obtained from a doctor or a dentist, or a pharmacist with a prescription from a Singapore-registered doctor or dentist.
Description
An inhibitor of DOPA decarboxylase, preventing conversion of levodopa to dopamine. It is used in parkinson disease to reduce peripheral adverse effects of levodopa. It has no antiparkinson actions by itself.
Indication
For treatment of the symptoms of idiopathic Parkinson's disease (paralysis agitans), post-encephalitic parkinsonism
Mechanism of Action
When mixed with levodopa, carbidopa inhibits the peripheral conversion of levodopa to dopamine and the decarboxylation of oxitriptan to serotonin by aromatic L-amino acid decarboxylase. This results in increased amount of levodopa and oxitriptan available for transport to the CNS. Carbidopa also inhibits the metabolism of levodopa in the GI tract, thus, increasing the bioavailability of levodopa.
Pharmacokinetics
- Absorption
- Rapidly decarboxylated to dopamine in extracerebral tissues so that only a small portion of a given dose is transported unchanged to the central nervous system.
- Distribution
- Metabolism
- The loss of the hydrazine functional group (probably as molecular nitrogen) represents the major metabolic pathway for carbidopa. There are several metabolites of carbidopa metabolism including 3-(3,4-dihydroxyphenyl)-2-methylpropionic acid, 3-(4-hydroxy-3-methoxyphenyl)-2-methylpropionic acid, 3-(3-hydroxyphenyl)-2-methylpropionic acid, 3-(4-hydroxy-3-methoxyphenyl)-2-methyllactic acid, 3-(3-hydroxyphenyl)-2-methyllactic acid, and 3,4-dihydroxyphenylacetone (1,2). [PMID: 4150141]
- Elimination
Toxicity
Symptoms of a carbidopa toxicity include muscle spasms or weakness, spasms of the eyelid, nausea, vomiting, diarrhea, an irregular heartbeat, confusion, agitation, hallucinations, and unconsciousness.
Active Ingredient/Synonyms
(-)-L-alpha-Hydrazino-3,4-dihydroxy-alpha-methylhydrocinnamic acid monohydrate | (S)-(−)-carbidopa | (S)-carbidopa | (αS)-α-hydrazino-3,4-dihydroxy-α-methylbenzenepropanoic acid | Carbidopa (anhydrous) | Carbidopa anhydrous | Carbidopum | L-3-(3,4-dihydroxyphenyl)-2-methyl-2-hydrazinopropionic acid | L-α-methyldopahydrazine | Carbidopa |
Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.
Description
The naturally occurring form of dihydroxyphenylalanine and the immediate precursor of dopamine. Unlike dopamine itself, it can be taken orally and crosses the blood-brain barrier. It is rapidly taken up by dopaminergic neurons and converted to dopamine. It is used for the treatment of parkinsonian disorders and is usually given with agents that inhibit its conversion to dopamine outside of the central nervous system.
Indication
For the treatment of idiopathic Parkinson's disease (Paralysis Agitans), postencephalitic parkinsonism, symptomatic parkinsonism which may follow injury to the nervous system by carbon monoxide intoxication, and manganese intoxication.
Mechanism of Action
Striatal dopamine levels in symptomatic Parkinson's disease are decreased by 60 to 80%, striatal dopaminergic neurotransmission may be enhanced by exogenous supplementation of dopamine through administration of dopamine's precursor, levodopa. A small percentage of each levodopa dose crosses the blood-brain barrier and is decarboxylated to dopamine. This newly formed dopamine then is available to stimulate dopaminergic receptors, thus compensating for the depleted supply of endogenous dopamine.
Pharmacokinetics
- Absorption
- Levodopa is rapidly absorbed from the proximal small intestine by the large neutral amino acid (LNAA) transport carrier system.
- Distribution
- Metabolism
- 95% of an administered oral dose of levodopa is pre-systemically decarboxylated to dopamine by the L-aromatic amino acid decarboxylase (AAAD) enzyme in the stomach, lumen of the intestine, kidney, and liver. Levodopa also may be methoxylated by the hepatic catechol-O-methyltransferase (COMT) enzyme system to 3-O-methyldopa (3-OMD), which cannot be converted to central dopamine.
- Elimination
Toxicity
Oral, mouse: LD50 = 2363 mg/kg; Oral, rabbit: LD50 = 609 mg/kg; Oral, rat: LD50 = 1780 mg/kg.
Active Ingredient/Synonyms
(−)-3-(3,4-dihydroxyphenyl)-L-alanine | (−)-dopa | 3-Hydroxy-L-tyrosine | 3,4-Dihydroxy-L-phenylalanine | Dihydroxy-L-phenylalanine | L-3,4-dihydroxyphenylalanine | L-beta-(3,4-Dihydroxyphenyl)alanine | L-DOPA | Levodopum | β-(3,4-dihydroxyphenyl)-L-alanine | β-(3,4-dihydroxyphenyl)alanine | Levodopa |
Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.