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Cabergoline Dopamine Receptor agonist

Cat.No.S5842

Cabergoline (FCE-21336), an ergot derivative, is a long-acting dopamine agonist and prolactin inhibitor.
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Quality Control

Batch: Purity: 99.82%
99.82

Solubility

In vitro
Batch:

DMSO : 90 mg/mL (199.29 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : 90 mg/mL

Water : Insoluble

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In vivo
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Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

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Chemical Information, Storage & Stability

Molecular Weight 451.60 Formula

C26H37N5O2

Storage (From the date of receipt) 3 years -20°C powder
CAS No. 81409-90-7 -- Storage of Stock Solutions

Synonyms FCE-21336 SMILES CCNC(=O)N(CCCN(C)C)C(=O)C1CC2C(CC3=CNC4=CC=CC2=C34)N(C1)CC=C

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Mechanism of Action

Targets/IC50/Ki
D2 receptor
0.7 nM
5-HT2
1.2 nM
5-HT2B
1.2 nM
D3 receptor
1.5 nM
D4 receptor
9 nM
In vitro
Cabergoline prevents the oxidative stress-induced cell death of cultured cortical neurons via a D2 receptor-mediated mechanism. This compound suppresses the activation of ERK signaling, which might have a role in the neuroprotection. It significantly represses extracellular glutamate accumulation triggered by oxidative stress, and increases the expression of glutamate transporters including EAAC1, which is known to be involved in the clearance of extracellular glutamate.
In vivo
Cabergoline has a long elimination half-life (63 to 109 h). An in vivo study of neuronal damage induced by intracerebroventricular (icv) injection of 6-OHDA, a neurotoxic compound that selectively damages dopaminergic neurons in male ICR mice, demonstrates that intraperitoneal (ip) administration of this compound for 7 days prevented nigrostriatal region dopaminergic neurons from cell death. It also protects SH-SY5Y neuroblastoma from cell death by oxygen-glucose deprivation even when this chemical is administered after the induction of cell death. This compound increases hippocampal brain-derived neurotrophic factor (BDNF, an important regulator in the synaptic plasticity) and exerts an antidepressant effect in rats.
References

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2025-09-23)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT07045935 RECRUITING
Prolactinoma
University Hospital, Basel, Switzerland
2025-09-16 PHASE4
NCT07034859 ENROLLING_BY_INVITATION
Pituitary Adenoma; MRI; RCT
National Taiwan University Hospital
2024-05-20 PHASE4
NCT07603466 ENROLLING_BY_INVITATION
Cushing Disease Due to Increased ACTH Secretion
University of Basrah
2026-05-11 PHASE4
NCT07568574 ENROLLING_BY_INVITATION
Safety and Impact of Medically Supervised Performance Enhancing Substance Usage in Healthy Elite Athletes
Enhanced Emirates Limited
2026-03-12
NCT07386080 NOT_YET_RECRUITING
Scizophrenia
Zealand University Hospital
2026-05-01 PHASE4
NCT07072910 RECRUITING
Migraine
Aarhus University Hospital
2025-11-12 PHASE2

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