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L-DOPA

Name: L-DOPA
Brand: TargetMol
SKU: T0848
Price: 50 USD
Availability: InStock
Rating: 5 (10 reviews)

(Synonyms: Levodopa, 3,4-Dihydroxyphenylalanine) Copy Product Info

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Synonyms: Levodopa, 3,4-Dihydroxyphenylalanine

Catalog No. T0848 Copy Product Info

Purity: 99.93%

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L-DOPA belongs to the category of dopamine precursors, serving as an orally active neurotransmitter metabolic precursor capable of crossing the blood-brain barrier and undergoing conversion to dopamine within the brain. The compound exhibits anti-hyperalgesic properties and finds application in Parkinson's disease research as well as in the induction of disease models.

Cas No. 59-92-7

Pack Size	Price	USA Stock	Global Stock	Quantity
200 mg	$50	In Stock	In Stock

For In stock only · Estimated delivery: USA Stock (1-2 days) Global Stock (5-7 days)

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For research use only—not for human use. No sales to individuals. Use as intended only.

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Purity:99.93%

Appearance:Solid

Color:White to Yellow

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COA HPLC HNMR

Product Introduction

Bioactivity

Description	L-DOPA belongs to the category of dopamine precursors, serving as an orally active neurotransmitter metabolic precursor capable of crossing the blood-brain barrier and undergoing conversion to dopamine within the brain. The compound exhibits anti-hyperalgesic properties and finds application in Parkinson's disease research as well as in the induction of disease models.
In vitro	Methods: C6 gliosarcoma cells were used to evaluate the antitumor activity of carborane-based L-DOPA compounds through in vitro survival assays (incubation with 20 ppm ¹⁰B for 6 h), cytotoxicity assays (continuous exposure for 3 d to determine IC50), and boron uptake assays (1.5 mM boron reagent culture for 24 h). Results: The carborane-based L-DOPA compound showed a minimum survival fraction of 0.03 after 75 min of thermal neutron irradiation, an IC50 of 8.93×10⁻⁴ M, and a cellular boron uptake of 1.53 μg/10⁷ cells, demonstrating superior in vitro killing effect compared to BSH.[1]
In vivo	Methods: A rat model with unilateral 6-OHDA lesion of the nigrostriatal pathway was established. Rats were administered L-DOPA (50 mg/kg, intraperitoneal injection, combined with benserazide 12.5 mg/kg, twice daily for 5-15 days). D3 receptor expression was detected by in situ hybridization and autoradiography, and rotational behavior was observed. Additionally, an MPTP-induced Parkinsonian monkey model was used to observe abnormal movements following L-DOPA administration. Results: Repeated L-DOPA administration induced ectopic expression of D3 receptors in the denervated caudate-putamen. This expression paralleled the time course of enhanced rotational behavior (behavioral sensitization), accompanied by upregulation of prodynorphin mRNA and downregulation of preprotachykinin mRNA. Various abnormal movements were also induced in the monkey model. [2] Methods: Intact rats were injected with L-DOPA (50 mg/kg) to measure endocannabinoid concentrations in the basal ganglia. In lesioned rats, L-DOPA-induced oro-lingual spontaneous movements were induced and treated with the cannabinoid agonist R(+)-WIN55,212-2 (1 mg/kg). Results: L-DOPA increased endocannabinoid concentrations in the basal ganglia and induced progressively severe oro-lingual spontaneous movements, which were attenuated by the cannabinoid agonist. [3] Methods: A rat model with unilateral severe 6-OHDA-induced lesion was used. L-DOPA was administered orally (25 mg/kg, combined with carbidopa, twice daily) for 6 months. Striatal D2 receptor binding levels were detected using 125I-sulpride autoradiography. Results: Chronic L-DOPA administration reversed the upregulation of D2 receptors in the caudate-putamen (particularly in the dorsolateral and ventrolateral regions) of severely lesioned rats, confirming that it reaches biologically active concentrations in the basal ganglia. [4]
Synonyms	Levodopa, 3,4-Dihydroxyphenylalanine
Disease Modeling Protocol	Parkinson's Disease (PD) Complications of Movement Model Modeling Mechanism： L-DOPA is a classic drug for treating Parkinson's disease, which is converted into dopamine in the brain to exert its replacement therapy effect. In a hemi-Parkinson's disease (hemi-PD) model constructed by unilateral destruction of striatal dopaminergic neurons with 6-hydroxydopamine (6-OHDA), due to the large number of dopaminergic neurons missing, the dopamine converted from exogenous L-DOPA cannot be reuptaken normally. It is mainly released non-specifically through serotonergic neurons, resulting in an abnormally high concentration of dopamine in the synaptic cleft. Excessive dopamine continuously overactivates downstream signaling of dopamine D1 receptors, leading to abnormal activation of the AKT/mTOR/S6K and CREB/ΔFosB pathways in the striatum (ST), ultimately inducing levodopa-induced dyskinesia (LID), thus simulating the core complication that occurs in clinical Parkinson's disease patients after long-term use of L-DOPA. Related Products： L-DOPA (T0848) Modeling Method： Experimental Subject： Mice: ICR strain, male, 6 weeks old, body weight 30–34 g Dosage and Administration Route： ① Core modelling (PD model establishment): 6-OHDA (8 μg/μL) dissolved in physiological saline containing 0.1% ascorbic acid, stereotaxically injected into the right striatum (coordinates: AP 0.5 mm anterior to the anterior fontanelle, ML 2.0 mm lateral, DV -3.0 mm depth), injection rate 0.5 μL/min,total volume 2 μL; sham group (SHAM): physiological saline containing 0.1% ascorbic acid, stereotaxic injection at identical coordinates; ② Core modelling (LID model induction): L-DOPA (80 mg/kg)+benzydamine (20 mg/kg) administered orally; ③ Group treatment: PD group: 6-OHDA lesionation only, no L-DOPA; LID group: 6-OHDA lesionation+L-DOPA+saline (vehicle control, oral); Positive control group: 6-OHDA lesionation+L-DOPA+amantadine (40 mg/kg, oral). Dosing Frequency and Duration Model： PD model establishment: Single injection on day 0; LID model induction and group treatment: Once daily from day 21 for 28 consecutive days Validation： 1. Behavioral Validation (Core Indicators): - Dyskinesia Score (AIMs Test): The total scores for axial, limb, oral, and motor dyskinesia were significantly higher in the LID group, peaking at 60 minutes, with the total AUC increasing ≥3 times compared to the PD group (p<0.001); - Motor Function Validation (Cylinder Test): The use rate of the contralateral forepaw in the PD group was significantly reduced (≥30% lower than in the SHAM group), recovering after L-DOPA intervention, and the 5-HTP/amantadine group did not affect the motor improvement efficacy of L-DOPA; 2. Molecular Indicators: - Signaling Pathways: The expression of striatal P-AKT (S473), P-mTOR (S2481), P-S6K (T389), P-CREB (S133), and ΔFosB proteins was 2-3 times higher than in the PD group (p<0.01); - Pathway Specificity: Did not affect D1/DARPP32/ERK Signal (distinguishing it from the mechanism of action of amantadine); 3. Histological verification: - Damage rate of striatal dopaminergic neurons ≥70% (verifiable by tyrosine hydroxylase TH immunohistochemistry). Precautions： One hour after L-DOPA administration on day 49, the patient was euthanized by cervical dislocation, and the right striatum was rapidly dissected. References：Choi Y,et,al. 5-Hydroxytryptophan Reduces Levodopa-Induced Dyskinesia via Regulating AKT/mTOR/S6K and CREB/ΔFosB Signals in a Mouse Model of Parkinson's Disease. Biomol Ther (Seoul). 2023 Jul 1;31(4):402-410.
Kinase Assay	Briefly, transfected HEK-293 cells, incubated in charcoal-treated Dulbecco's modified Eagle's medium for 24 h, are washed once with Hanks' solution and resuspended in a buffer containing 100 mM NaCl, 1 mM MgCl2, 1 mM EDTA, 1 mM EGTA, 250 mMsucrose, 20 mM Tris-HCl, pH 7.4. Cells are lysed by freezing in liquid nitrogen. Dehydrogenase activity is measured in a final volume of 20 μL containing the appropriate concentration of bile acid, 30 nCi of [3H]cortisol, and unlabeled cortisol to a final concentrations of 50 nM. The reaction is started by mixing cell lysate with the reaction mixture. Alternatively, endoplasmic reticulum microsomes are prepared from transfected HEK-293 cells and incubated with reaction mixture containing various concentrations of cortisol and CDCA. Incubation proceeded for 20 min, and the conversion of cortisol to cortisone is determined by thin layer chromatography (TLC). Because of the inaccuracy of the TLC method at low conversion rates and the end-product inhibition of 11βHSD2 at conversion rates higher than 60-70%, only conversion rates between 10 and 60% are considered for calculation. The inhibitory constant IC50 is evaluated using the curve-fitting program. Results are expressed as means±S.E. and consist of at least four independent measurements.

Chemical Properties

Molecular Weight	197.19
Formula	C₉H₁₁NO₄
Cas No.	59-92-7
Smiles	N[C@@H](Cc1ccc(O)c(O)c1)C(O)=O
Relative Density.	1.3075 g/cm3 (Estimated)

Storage & Solubility Information

Storage

Powder: -20°C for 3 years Shipping with blue ice/Shipping at ambient temperature.

Solubility Information

DMSO: Insoluble

H2O: 2.5 mM, Sonication is recommended.

Solution Preparation Table

H2O

	1mg	5mg	10mg	50mg
1 mM	5.0713 mL	25.3563 mL	50.7125 mL	253.5626 mL

Note : The dilution table applies only to solid products. For liquid products, please calculate the stock solution based on the stated concentration and/or density.

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10% DMSO+ 40% PEG300+ 5% Tween 80+ 45% Saline/PBS/ddH₂O , the resulting working solution concentration would be 2 mg/mL.

Stock Solution Preparation:

Dissolve 2 mg of the compound in 100 μL DMSO TargetMol | reagent to obtain a stock solution at a concentration of 20 mg/mL . If the required concentration exceeds the compound's known solubility, please contact us for technical support before proceeding.

Preparation of the In Vivo Formulation:

1) Add 100 μL of the DMSO TargetMol | reagent stock solution to 400 μL PEG300 and mix thoroughly until the solution becomes clear.

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