Citicoline
Based on 5 publication(s) in Google Scholar
Citicoline is an endogenous intermediate in the synthesis of phosphatidylcholine which is a component of cell membranes. Citicoline inhibits reactive oxygen species (ROS) and apoptosis. Citicoline can be used for neurological disease and hearing loss study.
For research use only. We do not sell to patients.
- Purity : 99.57%
- CAS No.: 987-78-0
- Formula: C14H26N4O11P2
- Molecular Weight:488.32
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Storage:Powder -20°C, 3 years , 4°C, 2 years
* The compound is unstable in solutions, freshly prepared is recommended.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Protocols
- Purity & Documentation
- References
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Help & FAQs
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Publications Citing Use of MedChemExpress (MCE) Citicoline
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Customer Validation & Images
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Others
All Endogenous Metabolite Isoforms
MoreAll Caspase Isoforms
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Biological Activity
Description
IC50 & Target
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Microbial Metabolite |
Human Endogenous Metabolite |
Caspase-8 |
Caspase-9 |
Caspase 3 |
In Vitro
Citicoline (1-100 μM, 24 h or 24 h before glutamate treatment) increases rats retinal cells viability after glutamate-induced excitotoxicity, and has synergistic effects with Tramiprosate (Homotaurine) (HY-14602)[1].
Citicoline (100 μM, 24 h before glutamate treatment and 30 min before HG treatment) decreases proapoptotic effects associated with neuroretinal degeneration such as glutamate-induced excitotoxicity and high glucose (HG)-induced neurotoxicity, and has synergistic effects with Tramiprosate in rats retinal cells[1].
Citicoline (100 μM, 36-48 h) reduces apoptosis in mice cochlear hair cells (HCs) and HEI-OC-1 cells after Neomycin (HY-150520) exposure, decreases the mRNA level of pro-apoptotic factor and increases anti-apoptotic factor, suppresses proapoptotic protein expression[2][3].
Citicoline (100 μM, 36-48 h) attenuates oxidative stress in mice cochlear HCs and HEI-OC-1 cells after Neomycin injury[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:Rat retinal cells
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Concentration:1, 10, 100 μM
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Incubation Time:24 h or 24 h before glutamate treatment (100 μM)
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Result:Did not affect viability of primary retinal cultures.
Significantly increased cell viability after glutamate-induced excitotoxicity, and had synergistic effects with homotaurine
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Cell Line:Rat retinal cells
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Concentration:100 μM
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Incubation Time:24 h before glutamate treatment and 30 min before HG treatment
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Result:Reduced apoptosis induced by administration of glutamate and HG, and had synergistic effects with homotaurine.
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Cell Line:HEI-OC-1, mice cochlear tissue
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Concentration:10 μM
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Incubation Time:36 or 48 h (pretreatment for 12 h and then treated with 10 mM neomycin together for 12 and 24 h in cochlear tissue and HEI-OC-1, respectively, then allowed to recover in culture medium for another 12
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Result:Showed significantly lower numbers of cleaved caspase 3-positive cells and TUNEL-positive cells than the neomycin-only group.
Significantly reduced the percentage of apoptosis.
The protein levels of cleaved caspase 3 were decreased compared with the Neomycin-only group.
Decreased the pro-apoptotic factor Bax, Casp3, Casp8, and Casp9, and increased anti-apoptotic factor Bcl-2 by qPT-PCR analysis.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Male C57Bl/6 mice (23-27 g) (The solution of convulsant pentylenetetrazole (1%) was infused intravenously at a flow rate of 0.01 ml/sec.)[2]
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Dosage:500, 1000 mg/kg
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Administration:Intraperitoneal injection (i.p.); 1 h before test
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Result:Increased the threshold of clonic seizures and tonic phase of seizures with lethal outcome in a dose of 500 mg/kg.
The anticonvulsant effect was most pronounced in a dose of 1000 mg/kg.
Chemical Information
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CAS No. 987-78-0
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Appearance Solid
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Molecular Weight 488.32
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Formula C14H26N4O11P2
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Color White to off-white
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SMILES
NC(C=CN1[C@H]2[C@H](O)[C@H](O)[C@@H](COP(OP(OCC[N+](C)(C)C)([O-])=O)(O)=O)O2)=NC1=O
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Synonyms
Cytidine diphosphate-choline; CDP-Choline; Cytidine 5'-diphosphocholine
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Powder -20°C 3 years 4°C 2 years * The compound is unstable in solutions, freshly prepared is recommended.
Publications (5)
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Journal Impact Factor
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Most Recent
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Nat Neurosci
2023 Apr;26(4):542-554. PMID: 36941428
Citicoline purchased from MedChemExpress. Usage Cited in: Nat Neurosci. 2023 Apr;26(4):542-554. [Abstract]
In vivo EEG and ex vivo MEA recordings of KA epileptic mice treated with CDP-choline (Citicoline: 100 mg/kg) or vehicle control.
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J Neuroinflammation
Microglial IRF7-induced lipophagy impairment aggravates lipid droplet overload and impedes neurological recovery after ischemic stroke. [Abstract]2026 Jun 17. PMID: 42310673 -
Int J Biol Macromol
2025 Mar:294:139536. PMID: 39765299 -
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Solvent & Solubility
In Vitro:
H2O : 50 mg/mL (102.39 mM; Need ultrasonic)
DMSO : < 1 mg/mL (insoluble or slightly soluble)
Please refer to the solubility information to select the appropriate solvent. The compound is unstable in solutions, freshly prepared is recommended.
* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.
Please refer to the solubility information to select the appropriate solvent. The compound is unstable in solutions, freshly prepared is recommended.
* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
In Vivo:
For the following dissolution methods, please prepare the working solution directly:
It is recommended to prepare fresh solutions and use them promptly within a short period of time.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Add each solvent one by one: PBS
Solubility: 50 mg/mL (102.39 mM); Clear solution; Need ultrasonic
Protocols
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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ROS/oxidative-stress fluorescent staining
ROS/oxidative-stress fluorescent staining uses cell-permeant fluorogenic probes that become fluorescent after oxidation inside cells or tissues; commonly used examples include DCFH-DA/DCFDA for broad cellular oxidant detection, DHE for superoxide-related signal detection, MitoSOX for mitochondrial superoxide-related signal detection, and CellROX probes for oxidative-stress-associated fluorescence readouts. The assay detects probe oxidation rather than a single ROS species unless the probe and analysis method have been chemically validated for that species. DCFH-DA enters cells, is deacetylated by intracellular esterases to DCFH, and produces fluorescent DCF after oxidation, so the readout is used as an operational measure of total cellular oxidative stress rather than a species-specific ROS measurement. DHE and MitoSOX can report superoxide-related oxidation, but red fluorescence alone can include non-specific ethidium-like oxidation products; HPLC or optimized spectral approaches are
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Research Protocol for Neurological Diseases
PINK1/Parkin-mediated mitophagy pathway is a mitochondrial quality-control signaling axis in which mitochondrial depolarization stabilizes PINK1 on damaged mitochondria, activates Parkin recruitment and E3 ubiquitin ligase activity, promotes ubiquitination of outer mitochondrial membrane proteins, recruits selective autophagy adaptors, and drives lysosomal degradation of damaged mitochondria. In neurological disease research, this pathway is experimentally important because neurons, especially dopaminergic neurons, are highly dependent on mitochondrial integrity, and defective mitochondrial turnover can lead to mitochondrial dysfunction, oxidative stress, impaired neuronal survival, α-synuclein accumulation, and neuroinflammatory damage-associated signals. The genetic disease link is strongest in Parkinson’s disease because mutations in PRKN/parkin cause autosomal recessive juvenile parkinsonism, mutations in PINK1 cause hereditary early-onset Parkinson’s disease, and Drosophila studie
Purity & Documentation
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Data Sheet (279 KB)
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SDS (396 KB)
- English - EN (396 KB)
- Français - FR (396 KB)
- Deutsch - DE (396 KB)
- Norwegian - NO (396 KB)
- Español - ES (396 KB)
- Swedish - SV (396 KB)
- Italian - IT (396 KB)
- Korean - KR (396 KB)
- Portuguese - PT (396 KB)
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Handling Instructions (2659 KB)
References
[1]. Davinelli S, et al. Cytoprotective Effects of Citicoline and Homotaurine against Glutamate and High Glucose Neurotoxicity in Primary Cultured Retinal Cells. Oxid Med Cell Longev. 2017;2017:2825703. [Content Brief]
[2]. Karpova MN, et al. Increase of the seizure threshold in C57BL/6 mice after citicoline administration. Bull Exp Biol Med. 2015 Jan;158(3):315-7. [Content Brief]
[3]. Zhong Z, et al. Citicoline Protects Auditory Hair Cells Against Neomycin-Induced Damage. Front Cell Dev Biol. 2020 Aug 31;8:712. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. The compound is unstable in solutions, freshly prepared is recommended.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
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| H2O | 1 mM | 2.0478 mL | 10.2392 mL | 20.4784 mL | 51.1959 mL |
| 5 mM | 0.4096 mL | 2.0478 mL | 4.0957 mL | 10.2392 mL | |
| 10 mM | 0.2048 mL | 1.0239 mL | 2.0478 mL | 5.1196 mL | |
| 15 mM | 0.1365 mL | 0.6826 mL | 1.3652 mL | 3.4131 mL | |
| 20 mM | 0.1024 mL | 0.5120 mL | 1.0239 mL | 2.5598 mL | |
| 25 mM | 0.0819 mL | 0.4096 mL | 0.8191 mL | 2.0478 mL | |
| 30 mM | 0.0683 mL | 0.3413 mL | 0.6826 mL | 1.7065 mL | |
| 40 mM | 0.0512 mL | 0.2560 mL | 0.5120 mL | 1.2799 mL | |
| 50 mM | 0.0410 mL | 0.2048 mL | 0.4096 mL | 1.0239 mL | |
| 60 mM | 0.0341 mL | 0.1707 mL | 0.3413 mL | 0.8533 mL | |
| 80 mM | 0.0256 mL | 0.1280 mL | 0.2560 mL | 0.6399 mL | |
| 100 mM | 0.0205 mL | 0.1024 mL | 0.2048 mL | 0.5120 mL |
* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.
Citicoline Related Classifications
HY-B0739 Related Classifications
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