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Carbidopa | CAS No: 28860-95-9 | GMP-certified suppliers
A medication that supports treatment of idiopathic and secondary parkinsonism and helps reduce levodopa‑related gastrointestinal symptoms in patients requiring flexible combination therapy.
Therapeutic categories
Primary indications
- Carbidopa is indicated with [levodopa] for the treatment of symptoms of idiopathic Parkinson disease, postencephalitic parkinsonism and symptomatic parkinsonism followed by carbon monoxide or manganese intoxication
- [FDA label]
- The combination therapy is administered for the reduction of [levodopa]-driven nausea and vomiting
- [FDA label]
Product Snapshot
- Carbidopa is an oral and enteral small‑molecule API supplied in multiple solid and gel formulations for combination use with levodopa
- It is used to support levodopa-based management of Parkinsonian symptoms and to reduce levodopa‑associated gastrointestinal effects
- The molecule is approved and marketed in the US, EU, and Canada
Clinical Overview
Carbidopa limits the peripheral conversion of levodopa to dopamine and reduces decarboxylation of other substrates such as oxitriptan. Because carbidopa does not cross the blood–brain barrier, its pharmacological activity is restricted to peripheral tissues, thereby increasing the fraction of administered levodopa that reaches the central nervous system. This effect increases levodopa bioavailability, prolongs its half‑life, reduces clearance, and decreases dopamine‑mediated gastrointestinal adverse effects. The pharmacodynamic effect is not strongly dose‑dependent within typical therapeutic ranges.
After oral administration, carbidopa reduces levodopa metabolism in the gastrointestinal tract and increases urinary recovery of unchanged levodopa, consistent with inhibition of peripheral enzymatic conversion. Its inability to enter the central nervous system ensures that it does not interfere with dopamine generation within the brain.
Safety considerations include the potential for levodopa‑related dyskinesia, orthostatic hypotension, and neuropsychiatric effects when used in combination therapy. Carbidopa alone may mitigate nausea in select patients, but it is not effective as monotherapy for motor symptoms. Dose adjustment of both components may be required in patients experiencing excessive dopaminergic effects. Carbidopa is mainly eliminated renally, and caution is advised in patients with impaired renal function.
Notable usage contexts include long‑standing global use of carbidopa and levodopa combination products originally developed by Mayne Pharma, with a standalone carbidopa tablet first approved in 2014 by Amerigens Pharmaceuticals.
For API procurement, sourcing should prioritize verified identity, control of hydrazine‑related impurities, and compliance with pharmacopeial specifications to support consistent performance in fixed‑dose and titratable formulations.
Identification & chemistry
| Generic name | Carbidopa |
|---|---|
| Molecule type | Small molecule |
| CAS | 28860-95-9 |
| UNII | KR87B45RGH |
| DrugBank ID | DB00190 |
Pharmacology
| Summary | Carbidopa inhibits peripheral aromatic L‑amino acid decarboxylase, reducing the conversion of levodopa to dopamine and other monoamines outside the central nervous system. By limiting peripheral metabolism and increasing levodopa bioavailability, it supports greater delivery of levodopa to the brain for dopaminergic replacement. Its action is restricted to the periphery because it does not cross the blood–brain barrier. |
|---|---|
| Mechanism of action | Carbidopa is an inhibitor of the DDC which in order, inhibits the peripheral metabolism of levodopa.DDC is very important in the biosynthesis of L-tryptophan to serotonin and the modification of L-DOPA to dopamine. DDC can be found in the body periphery and in the blood-brain barrier.The action of carbidopa is focused on peripheral DDC as this drug cannot cross the blood-brain barrier.Hence, it will prevent the metabolism of [levodopa] in the periphery but it will not have any activity on the generation of dopamine in the brain. |
| Pharmacodynamics | 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 an increased amount of [levodopa] and [oxitriptan] available for transport to the central nervous system. Carbidopa also inhibits the metabolism of [levodopa] in the GI tract, thus, increasing the bioavailability of [levodopa]. The presence of additional units of circulating [levodopa] can increase the effectiveness of the still functional dopaminergic neurons and it has been shown to alleviate symptoms for a time. The action of carbidopa is very important as [levodopa] is able to cross the blood-brain barrier while dopamine cannot.Hence the administration of carbidopa is essential to prevent the transformation of external [levodopa] to dopamine before reaching the main action site in the brain. The coadministration of carbidopa with [levodopa] has been shown to increase the half-life of [levodopa] more than 1.5 times while increasing the plasma level and decreasing clearance. The combination therapy has also shown an increase of the recovery of [levodopa] in urine instead of dopamine which proves a reduced metabolism. This effect has been highly observed by a significant reduction in [levodopa] requirements and a significant reduction in the presence of side effects such as nausea. It has been observed that the effect of carbidopa is not dose-dependent. |
Targets
| Target | Organism | Actions |
|---|---|---|
| Aromatic-L-amino-acid decarboxylase | Humans | inhibitor |
ADME / PK
| Absorption | When [levodopa]/carbidopa is administered orally, 40-70% of the administered dose is absorbed.Once absorbed, carbidopa shows bioavailability of 58%.A maximum concentration of 0.085 mcg/ml was achieved after 143 min with an AUC of 19.28 mcg.min/ml. |
|---|---|
| Half-life | The reported half-life of carbidopa is of approximately 107 minutes. |
| Protein binding | It is widely accepted that the protein binding of carbidopa is 76%. However, more studies are required or the presentation of the source of this information. |
| 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). |
| Route of elimination | In animal studies, 66% of the administered dose of carbidopa was eliminated via the urine while 11% was found in feces. These studies were performed in humans and it was observed a urine excretion covering 50% of the administered dose. |
| Volume of distribution | The volume of distribution reported for the combination therapy of carbidopa/[levodopa] is of 3.6 L/kg.However, carbidopa is widely distributed in the tissues, except in the brain.After one hour, carbidopa is found mainly in the kidney, lungs, small intestine and liver. |
| Clearance | The reported clearance rate for the combination therapy of [levodopa]/carbidopa is 51.7 L/h. |
Formulation & handling
- Oral and enteral formulations leverage its hydrophilic small‑molecule profile, with extended‑release forms requiring matrix systems to control rapid dissolution.
- Aqueous solubility supports suspension or gel formulations, but solution forms require protection from oxidation and light to limit degradation.
- Handling of the solid API should minimize moisture exposure due to its hygroscopic and stability‑sensitive nature during processing.
Regulatory status
| Lifecycle | The API is in a mature market phase in Canada, the US, and the EU, with early patents expiring in 2020 and later US patents extending protection through 2028. Market dynamics are likely shaped by partial patent expiry and remaining exclusivities that continue to limit full generic competition in the US. |
|---|
| Markets | Canada, US, EU |
|---|
Supply Chain
| Supply chain summary | Carbidopa appears to have a limited set of originator‑level manufacturers, with additional downstream packagers supporting distribution across the US, EU, and Canada. The presence of multiple branded formulations in all three regions indicates established global market availability. Several key patents expired in 2020, while others extend to 2028, suggesting that generic competition is already present alongside remaining protected products. |
|---|
Safety
| Toxicity | The LD50 of carbidopa is reported to be in the rat of 4810 mg/kg.[MSDS] In animal studies, carbidopa showed no incidences on neoplasia and showed no effect on the fertility status and development.[FDA label] No reports of overdosage have been registered with the carbidopa-only product. In the event of overdosage, immediate gastric lavage is recommended as well as intravenous fluid administration. Continuous electrocardiographic monitoring is required.[FDA label] |
|---|
- Rat oral LD50 is reported at 4810 mg/kg, indicating relatively low acute toxicity
- No neoplasia or fertility effects were observed in animal studies
- No overdosage cases have been documented for carbidopa alone, but excessive exposure may warrant controlled clinical monitoring due to potential cardiovascular effects
Carbidopa is a type of Nervous System Agents
Nervous System Agents are a crucial subcategory of pharmaceutical active pharmaceutical ingredients (APIs) that target the intricate workings of the nervous system. These agents play a pivotal role in managing various neurological conditions and disorders by modulating the neurotransmitters and receptors involved in nerve signaling.
Nervous System Agents encompass a wide range of pharmaceutical APIs, including but not limited to antiepileptic drugs, antidepressants, antipsychotics, anxiolytics, and analgesics. These APIs work by interacting with specific molecular targets in the nervous system, such as neurotransmitter receptors or enzymes involved in neurotransmitter synthesis or degradation.
One notable class of Nervous System Agents is CGRP (Calcitonin Gene-Related Peptide) antagonists. CGRP is a neuropeptide involved in the transmission of pain signals in the central and peripheral nervous systems. CGRP antagonists act by blocking the CGRP receptors, thereby inhibiting the CGRP-mediated pain pathway.
CGRP antagonists have shown promising therapeutic potential in the management of migraine headaches. By selectively targeting CGRP receptors, these pharmaceutical APIs can effectively prevent or reduce the frequency and severity of migraines. They offer an alternative treatment option for patients who do not respond well to conventional migraine medications.
The development and utilization of Nervous System Agents, including CGRP antagonists, represent a significant advancement in the field of neuropharmacology. These APIs provide healthcare professionals with valuable tools to address various neurological disorders, ultimately improving patients' quality of life. Continued research and innovation in this subcategory are expected to lead to further breakthroughs in the treatment of nervous system-related conditions.
Carbidopa (Nervous System Agents), classified under Central Nervous System Agents
Central Nervous System (CNS) Agents are a crucial category of pharmaceutical Active Pharmaceutical Ingredients (APIs) that specifically target the central nervous system. The CNS encompasses the brain and spinal cord, playing a vital role in regulating and controlling various bodily functions, including cognition, movement, emotions, and sensory perception. These agents are designed to interact with specific receptors, enzymes, or ion channels within the CNS to modulate neural activity and restore normal functioning.
CNS agents comprise a diverse range of pharmaceutical APIs, including analgesics, anesthetics, antipsychotics, sedatives, hypnotics, anti-epileptics, and antidepressants. Each subcategory addresses distinct neurological disorders and conditions. For instance, analgesics alleviate pain by targeting receptors in the brain and spinal cord, while antipsychotics are employed to manage psychosis symptoms in mental illnesses such as schizophrenia.
The development of CNS agents involves rigorous research, molecular modeling, and extensive clinical trials to ensure safety, efficacy, and specific target engagement. Pharmaceutical companies invest significant resources in identifying novel drug targets, synthesizing new compounds, and optimizing their pharmacological properties. These agents undergo rigorous regulatory evaluations and must adhere to stringent quality standards and guidelines.
Given the prevalence of CNS disorders globally, the market demand for effective CNS agents is substantial. The development of innovative CNS APIs not only improves patient outcomes but also provides valuable commercial opportunities for pharmaceutical companies. Continued advancements in CNS agent research and development hold the promise of groundbreaking therapies that can improve the quality of life for individuals affected by neurological conditions.
Carbidopa API manufacturers & distributors
Compare qualified Carbidopa API suppliers worldwide. We currently have 11 companies offering Carbidopa API, with manufacturing taking place in 5 different countries. Use the table below to review supplier type, countries of origin, certifications, product portfolio and GMP audit availability.
| Supplier | Type | Country | Product origin | Certifications | Portfolio |
|---|---|---|---|---|---|
| Apollo Healthcare Resourc... | Distributor | Singapore | Singapore | BSE/TSE, CEP, CoA, EDMF/ASMF, FDA, GMP, ISO9001, JDMF, KDMF, MSDS, USDMF, WC | 200 products |
| Divis Labs. | Producer | India | India | CEP, CoA, FDA, GMP, ISO9001, Other, JDMF, KDMF, USDMF, WC | 47 products |
| Duchefa Farma B.V. | Distributor | Netherlands | India | CoA, GMP, ISO9001, MSDS | 170 products |
| Fermion | Producer | Finland | Finland | BSE/TSE, CEP, CoA, GDP, GMP, MSDS, USDMF | 29 products |
| Glochem | Producer | India | India | CoA, FDA, GMP, USDMF, WC | 14 products |
| Shandong Xinhua | Producer | China | China | CEP, CoA, FDA, GMP, JDMF, USDMF, WC | 21 products |
| Sicor | Producer | Italy | Italy | CoA, GMP | 47 products |
| Sinoway industrial Co.,Lt... | Distributor | China | China | CEP, CoA, GMP, ISO9001, MSDS, USDMF | 762 products |
| Tenatra Exports Private L... | Distributor | India | India | BSE/TSE, CoA, FDA, GMP, MSDS | 263 products |
| Zhejiang Chiral M.C. | Producer | China | China | CEP, CoA, FDA, GMP, USDMF, WC | 4 products |
| Zhejiang Wild Wind | Producer | China | China | CEP, CoA, USDMF, WC | 4 products |
When sending a request, specify which Carbidopa API quality you need: for example EP (Ph. Eur.), USP, JP, BP, or another pharmacopoeial standard, as well as the required grade (base, salt, micronised, specific purity, etc.).
Use the list above to find high-quality Carbidopa API suppliers. For example, you can select GMP, FDA or ISO certified suppliers. Visit our help page to learn more about sourcing APIs via Pharmaoffer.
Frequently asked questions about Carbidopa API
Sourcing
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Technical
What is Carbidopa (CAS 28860-95-9) used for?
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How does Carbidopa work?
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Is Carbidopa a small molecule?
Are there special stability concerns for oral Carbidopa?
Regulatory
Where is Carbidopa approved or in use globally?
Pharmaoffer
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