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Fig. 1 · Structure
Cat. No.
A10181
CAS No.
28860-95-9
Formula
C10H14N2O4
Mol. Weight
226.2

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Carbidopa

Cat. No. A10181 CAS 28860-95-9

aromatic-L-amino-acid decarboxylase inhibitor

Carbidopa inhibits aromatic-L-amino-acid decarboxylase, an enzyme important in the biosynthesis of L-tryptophan to serotonin and in the biosynthesis of L-DOPA to Dopamine (DA).

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Biological Activity

Bioactivity / Mechanism

Carbidopa engages the PLP-dependent human DOPA decarboxylase active site through a PLP-linked hydrazone. Spectroscopic and crystallographic evidence supports a bound ketoenamine form; these experiments characterize target engagement rather than an enzyme IC50. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

In Vitro Studies

In a 24 h MTT assay, carbidopa reduced viability in LNCaP and VCAP prostate cancer cells, with reported cellular IC50 values of 68 and 71 μM. DU145 and PC3 cells showed much less response under the same conditions, limiting generalization across cell models. [2]

Spectroscopic characterization of the carbidopa–PLP adduct

Biochemical assay · Human DOPA decarboxylase (hDdc) and free pyridoxal phosphate (PLP) [1]

Carbidopa produced a PLP-hydrazone spectral signature in hDdc. Unlike free PLP in solution, the enzyme favored the ketoenamine form at both tested pH values. This is binding/adduct evidence, not an enzyme IC50 determination.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
hDdc-bound carbidopa hydrazone spectral maximaAbsorbance maximum 384 nm at pH 6; 396 nm at pH 8[1]

Literature-Reported Treatment Conditions

Treatment concentration
hDdc spectra: 2 mM carbidopa. Free-PLP comparison: 50 μM PLP with 100 μM carbidopa.
Exposure duration
hDdc: 30 min; free-PLP scans every 60 s for 1 h.
Method
Absorbance spectra at pH 6 and 8; physiological-pH absorbance/CD in Figure 4C insets.
Reported limits
No enzyme activity IC50 is established by this selected experiment; replication and uncertainty for spectral maxima are not specified in the read main-text locations.
Methods and source locations

Compound reported in the paper: Carbidopa

Compound-level research evidence; no Adooq lot validation or clinical efficacy claim.

Results and Discussion: human carbidopa paragraphs; Figure 4A–D and caption; Methods: Stopped-Flow Spectrophotometric Studies

hDdc-bound carbidopa hydrazone spectral maxima: UV–visible absorbance; maxima stated in original text, not estimated from the image. — Results and Discussion: paragraph beginning “Extending our study”; Figure 4C and caption

Crystal structure of human DDC bound to carbidopa

Biochemical assay · Human holo-DOPA decarboxylase–carbidopa complex, PDB 9GNS [1]

The X-ray structure supports a PLP-linked carbidopa hydrazone in the ketoenamine form. It provides a structural basis for target engagement; it does not measure cellular potency or therapeutic benefit.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Resolution of the human DDC–carbidopa crystal structureX-ray resolution 1.93 Å[1]

Literature-Reported Treatment Conditions

Treatment concentration
Carbidopa supplied in ligand excess, described as 10 × protein concentration.
Exposure duration
2 h crystal soaking.
Method
X-ray crystallography; ligand modeled against an unliganded human holoDdc structure (8OR9).
Reported limits
SI Table S16 and Figure S6 not retrieved. Methods give pH 7.5 crystallization buffer, while Results describe the complex at pH 7.4; neither is silently substituted for the other.
Methods and source locations

Compound reported in the paper: Carbidopa

Compound-level research evidence; no Adooq lot validation or clinical efficacy claim.

Methods: Crystallization of hDdc, X-ray Data Collection and Processing, Structure Determination and Refinement; Results final human-DDC paragraph; Figure 5

Resolution of the human DDC–carbidopa crystal structure: X-ray diffraction; reported main-text resolution; PDB 9GNS. — Results and Discussion: paragraph beginning “The crystallographic structure”; Figure 5

Cell-line-dependent viability response in prostate cancer cells

Cell-based study · Human LNCaP and VCAP prostate cancer cells, with DU145 and PC3 comparators [2]

After 24 h, MTT concentration-response assays showed reduced viability in LNCaP and VCAP cells, with substantially less response in DU145 and PC3. This model-specific response does not establish general anticancer efficacy.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Reduction in MTT viability of LNCaP and VCAP cellsCellular IC50 LNCaP: 68 μM; VCAP: 71 μM[2]
Response of DU145 and PC3 comparator cell linesComparative viability response Almost no effect reported in DU145 and PC3 under the same assay conditions[2]

Literature-Reported Treatment Conditions

Treatment concentration
0–200 μM carbidopa.
Exposure duration
24 h drug exposure.
Method
MTT readout at 490 nm after 4 h with MTT; cells assayed in phenol-red-free medium.
Reported limits
Drug vehicle, compound lot and MTT biological replicate count are not specified in the selected text/caption. DMSO used to dissolve formazan is not assigned as the treatment vehicle.
Methods and source locations

Compound reported in the paper: Carbidopa

Compound-level research evidence; no Adooq lot validation or clinical efficacy claim.

Results: Carbidopa inhibits LNCaP and VCAP cell proliferation…; Figure 1c,e; Methods: Cell culture, Cell proliferation assay, Statistical analysis

Reduction in MTT viability of LNCaP and VCAP cells: 24 h MTT concentration-response assay; values reported in Results. These are cellular assay endpoints, not treatment doses or enzyme IC50 values. — Results first subsection, Figure 1c,e and caption; Cell proliferation assay

Response of DU145 and PC3 comparator cell lines: MTT; Figure 1c,e viewed. Small changes visible in comparator curves are not converted into exact percentages or described as proof of complete inactivity. — Results first subsection and Figure 1c,e

In Vivo Studies

In anesthetized rats, carbidopa pretreatment increased total levodopa recovered in blood and striatal microdialysate to 3.5 and 8.0 times the levodopa-alone values. The result concerns acute coadministration and dialysate pharmacokinetics; it does not establish carbidopa monotherapy efficacy. [3]

Carbidopa pretreatment changes levodopa recovery in rat microdialysate

Animal study · Male Slc:Wistar rats, 8 weeks, 280–320 g, under urethane anesthesia; blood and striatal microdialysis [3]

Carbidopa given before levodopa increased the total amount of levodopa recovered from blood and striatal dialysate relative to levodopa alone. This is an acute combination pharmacokinetic result, not carbidopa monotherapy efficacy.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Total levodopa recovered in dialysate relative to levodopa aloneReported total-amount ratio Blood: 3.5-fold; striatum: 8.0-fold[3]

Conditions shared by the study groups

Route
Intraperitoneal for both compounds.
Frequency
Single carbidopa pretreatment; levodopa 40 min later.
Treatment course
Acute study; samples collected every 20 min over the stated 6- or 10-h observation window.
Vehicle
Acidified saline.
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Carbidopa followed by levodopa
Carbidopa 25 μmol/kg; L-Dopa 250 μmol/kg.		Levodopa alone with vehicle pretreatment; benserazide 25 or 62.5 μmol/kg with levodopa as active comparators; vehicle-only controls also described.Levodopa dialysate total-amount ratios were 3.5 in blood and 8.0 in striatum versus levodopa alone. Benserazide 62.5 μmol/kg gave ratios of 5.5 and 6.1 respectively. Carbidopa was detectable in blood but never detected in striatal dialysate.[3]
Carbidopa followed by levodopa
Model: Male Slc:Wistar rats, 8 weeks, 280–320 g, under urethane anesthesia; blood and striatal microdialysis
Reported limits: This is drug recovery into dialysate, not absolute brain drug exposure or motor-function efficacy. No claim of superiority in patients is supported.
Methods and source locations

Compound reported in the paper: Carbidopa

Compound-level research evidence; no Adooq lot validation or clinical efficacy claim.

pp. 988–990 Materials and Methods/Results; Figure 1; Table 2; pp. 991–993 comparator and detection results

Total levodopa recovered in dialysate relative to levodopa alone: Moment analysis; Table 2 n = 4–5, underlying quantities reported as mean ± SD. Fold ratios have no separately reported uncertainty. Both increases marked p < 0.05 versus levodopa alone. — p. 990 Table 2 and adjacent Results; Figure 1

Carbidopa followed by levodopa · p. 989 Animal Experiments; p. 990 Figure 1/Table 2; pp. 992–993 striatal detection statement

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 28860-95-9
Applications aromatic-L-amino-acid decarboxylase inhibitor
Formula C10H14N2O4
Molecular Weight 226.2
Synonyms Lodosyn
SMILES
C[C@](CC1=CC(=C(C=C1)O)O)(C(=O)O)NN

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 3 mg/mL (13.26 mM)
Water Insoluble
Ethanol Insoluble

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

In Vivo Preparation

Concentration
1 mg/mL
Vehicle
4% DMSO+30% PEG 300+2% Tween 80+ddH2O

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Jonathan M. Baine, Yoan Duhoo, Tzanko Doukov, et al. α-Hydrazino Acids Inhibit Pyridoxal Phosphate-Dependent Decarboxylases via “Catalytically Correct” Ketoenamine Tautomers: A Special Motif for Chemical Biology and Drug Discovery? ACS Catalysis (2025). PMID: 40401103 DOI: 10.1021/acscatal.5c00326 Source material
  2. [2] Zhiwei Chen, Aimin Cai, Hailun Zheng, et al. Carbidopa suppresses prostate cancer via aryl hydrocarbon receptor-mediated ubiquitination and degradation of androgen receptor Oncogenesis (2020). PMID: 32404918 DOI: 10.1038/s41389-020-0236-x Source material
  3. [3] Mikiro Nakashima, Mei Feng Zhao, Mihoko N. Nakashima, et al. In Vivo Microdialysis to Determine the Relative Pharmacokinetics of Drugs Biological and Pharmaceutical Bulletin (1996). PMID: 8839975 DOI: 10.1248/bpb.19.988 Source material

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