Art. -Nr.: HY-N21834

Erysodine

Erysodine is a blood-brain barrier-permeable nicotinic acetylcholine receptor (nAChR) ligand with high affinity for α4β2 nAChR, K_i= 5 nM, and it blocks nicotine-induced dopamine release and behavioral effects through competitive inhibition. Erysodine is useful for studies on alcohol dependence.

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CAS. Nr.: 7290-03-1
Formel: C₁₈H₂₁NO₃
Molecular Weight:299.37

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Erysodine Chemical Structure

CAS. Nr.: 7290-03-1

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Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biologische Aktivität
- Beschreibung
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- Parmacokinetics
- In Vivo
Chemical Information
Reinheit & Dokumentation
Verweise
Calculators
Help & FAQs
Classifications
Bioz

Biologische Aktivität

Beschreibung

IC₅₀ & Target

^[4]

nAChR

5 nM (Ki)

Cellular Effect

Cell Line	Type	Value	Description	References
IMR-32	IC50	7 μM	Inhibition of (-)-nicotine-induced ⁸⁶Rb⁺ efflux from IMR-32 human neuroblastoma cells measured by ⁸⁶Rb⁺ efflux assay. Inhibition of (-)-nicotine-induced ⁸⁶Rb⁺ efflux from IMR-32 human neuroblastoma cells measured by ⁸⁶Rb⁺ efflux assay.	7498257

In Vitro

Erysodine (2.5-100 nM) is a high-affinity competitive inhibitor of [³H]cytisine binding at the α₄β₂ neuronal nicotinic acetylcholine receptor subtype in rat brain cell membranes^[1].
Erysodine (3 h) exhibits significantly lower affinity for α-bungarotoxin-sensitive neuronal nicotinic acetylcholine receptor subtypes in rat brain compared to its affinity for the α₄β₂ subtype labeled by [³H]cytisine, with a K_ivalue of 4000 nM^[1].
Erysodine (7 μM) is a functional antagonist of nicotinic acetylcholine receptor-mediated cation efflux in IMR-32 human neuroblastoma cells^[1].
Erysodine is a potent competitive antagonist of the α4β2 nicotinic acetylcholine receptor, with a K_i of 5 nM for the displacement of [³H]-cytisine in brain membrane fractions^[4].
Erysodine potently blocks acetylcholine-induced activation of α4β2 nicotinic acetylcholine receptor currents, with an IC₅₀ of 20 nM^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Parmacokinetics

Species	Dose	Route	Brain Concentration	Plasma Concentration
Mice^[1]	10 μM/kg	i.p.	58 ng/g	21 ng/mL
Mice^[1]	30 μM/kg	i.p.	280 ng/g	/
Mice^[1]	30 μM/kg	i.p.	92.2 ng/g	30.5 ng/mL

In Vivo

Erysodine (3-30 μmol/kg; i.p.; administered 5 min before (-)-nicotine challenge) penetrates the brain systemically in CD-1 mice and dose-dependently antagonizes nicotine-induced hypothermia and anxiolytic-like responses, with no overt toxicity observed at 3 times the minimum effective antagonist dose^[1].
Erysodine (30 μmol/kg; i.p.; administered 5 min before (-)-nicotine challenge) penetrates the blood-brain barrier in Wistar rats and completely blocks the biphasic effects (initial inhibition, subsequent excitation) of (-)-nicotine on locomotor activity and rearing behavior^[1].
Erysodine (0.3-10 mg/kg; s.c.; administered 15 min before testing) is a surmountable competitive antagonist of the nicotine discriminative stimulus, producing up to a 9-fold rightward shift in nicotine potency at a dose of 1.0 mg/kg, with minimal disruption of operant response rates^[3].
Erysodine (0.32-32 mg/kg; s.c.; administered 15 min before the 90-min test session) dose-dependently and selectively reduces nicotine self-administration behavior under a fixed-ratio 5 schedule, with the maximum effect at the highest tested dose being comparable to full nicotine antagonism^[3].
Erysodine (0.1-10 mg/kg; s.c.; administered 15 min before the 3 h test session) dose-dependently reduces the progressive ratio breakpoint for nicotine self-administration, without producing nonspecific effects on response latency during the test session^[3].
Erysodine (1.5-8 mg/kg; i.p.; once daily for 3 consecutive days) dose-dependently reduces voluntary ethanol intake and ethanol preference in alcohol-preferring UChB rats, with a daily dose of 8.0 mg/kg decreasing ethanol intake by an average of 66% during the treatment period and the initial post-dosing phase^[4].
Erysodine (10 mg/kg; i.p.; single injection) does not alter locomotor activity in healthy male Sprague-Dawley rats, indicating that the previously observed reduction in ethanol intake is not due to a motor-impairing effect of this compound^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

CD-1 mice (Male, 30-35 g)^[1]
Dosage:

3 μmol/kg; 10 μmol/kg; 30 μmol/kg
Administration:

i.p.; 5 min prior to (-)-nicotine challenge
Result:

Showed no significant nicotine-induced hypothermia in mice pretreated with 10 μmol/kg or 30 μmol/kg erysodine.
Attenuated the tendency for (-)-nicotine to reduce locomotor activity at 30 μmol/kg.
Did not alter time spent in the open arms of the elevated plus-maze on its own at 30 μmol/kg, but fully blocked the anxiolytic-like increase in open arm time induced by (-)-nicotine.
Reached 58 ng/g brain levels and 21 ng/mL plasma levels at 15 minutes after 10 μmol/kg i.p. administration.
Reached 92.2 ng/g brain levels and 30.5 ng/mL plasma levels immediately after elevated plus-maze testing.
Showed no obvious toxicities following administration of 30 μmol/kg erysodine.

Animal Model:

Wistar rats (Male, 250-300 g)^[1]
Dosage:

30 μmol/kg
Administration:

i.p.; 5 min prior to (-)-nicotine challenge
Result:

Did not significantly alter rearing behavior at the 10 min (maximal nicotine-induced locomotor suppression) or 40 min (maximal nicotine-induced locomotor stimulation) post-nicotine time points.
Prevented the early developing (-)-nicotine-induced decrease in both horizontal activity and rearing at 10 min, and also prevented the late developing (-)-nicotine-induced increase in both horizontal activity and rearing at 40 min.
Reached 280 ng/g brain concentrations at 10 min and 306 ng/g at 40 min post-administration, with a corresponding brain:plasma ratio of 1.5 at 10 min.

Animal Model:

Sprague-Dawley rats (adult male, initial weight 250-275 g, held at ~350 g via restricted feeding during training)^[3]
Dosage:

0.3 mg/kg; 1.0 mg/kg; 10 mg/kg
Administration:

s.c.; 15 min prior to test sessions
Result:

Produce a dose-dependent, complete blockade of the nicotine discriminative stimulus when co-administered with 0.4 mg/kg nicotine training dose, and 10 mg/kg administered alone does not substitute for nicotine.
Shift the nicotine dose-response curve ~6-fold rightward at 0.3 mg/kg, resulting in a nicotine ED₅₀ of 0.31 mg/kg.
Shift the nicotine dose-response curve ~9-fold rightward at 1.0 mg/kg, resulting in a nicotine ED₅₀ of 0.43 mg/kg.
Cause no substantial reductions in session response rates for most erysodine + nicotine combinations.

Animal Model:

Long-Evans rats (adult male, initial weight 250-275 g)^[3]
Dosage:

0.32 mg/kg; 3.2 mg/kg; 32 mg/kg
Administration:

s.c.; 15 min prior to 90-minute test sessions
Result:

Produce a dose-dependent reduction in nicotine self-administration that selectively decreases nicotine-reinforced responding without affecting food-maintained response rates.
Reach a maximal decrease of ~50-60% in nicotine self-administration, matching the level of reduction observed during saline extinction conditions.

Animal Model:

Long-Evans rats (adult male)^[3]
Dosage:

0.1 mg/kg; 0.32 mg/kg; 1.0 mg/kg; 3.2 mg/kg; 10 mg/kg
Administration:

s.c.; 15 min prior to 3-hour test sessions
Result:

Produce dose-dependent decreases in progressive-ratio break points relative to vehicle control (mean vehicle break point 54.6), with break points reduced to a mean of 43.1 at 10 mg/kg.
Do not systematically alter latencies to complete the first, fifth, or break-point infusions.

Animal Model:

Wistar-UChB rats (Adult male, 250-300 g body weight, alcohol-preferring, two-bottle 24 h free choice access paradigm)^[4]
Dosage:

1.5 mg/kg; 2.0 mg/kg; 4.0 mg/kg; 8.0 mg/kg
Administration:

i.p.; per day; 3 consecutive days
Result:

Produced a dose-dependent reduction in ethanol consumption.
Reduced average 3-day treatment ethanol intake by 23% at 1.5 mg/kg, with reduction in ethanol intake observed only on the third day of treatment.
Reduced average 3-day treatment ethanol intake by 29% at 2.0 mg/kg, with reduction in ethanol intake observed only on the second day of treatment.
Reduced average ethanol intake by 45% over the treatment period and the first post-treatment day at 4.0 mg/kg, with reductions in ethanol preference seen during the second and third treatment days and first post-treatment day.
Reduced average ethanol intake by 66% over the full treatment period and first post-treatment day at 8.0 mg/kg, with reductions in ethanol preference observed across all 3 treatment days and the first post-treatment day.
Showed no observable signs of animal discomfort in treated rats.

Animal Model:

Sprague-Dawley rats (Male, healthy)^[4]
Dosage:

10 mg/kg
Administration:

i.p.; single injection
Result:

Showed cumulative total distance traveled and time-course locomotor activity after 10 mg/kg administration equivalent to that of saline-treated control animals.

Chemical Information

CAS. Nr. 7290-03-1
Molecular Weight 299.37
Formel C₁₈H₂₁NO₃
SMILES

O(C)[C@@H]1C[C@]23C=4C(CCN2CC=C3C=C1)=CC(O)=C(OC)C4
Structure Classification
- Alkaloids
- Other Alkaloids
Initial Source
Versand

Room temperature in continental US; may vary elsewhere.
Speicherung

Please store the product under the recommended conditions in the Certificate of Analysis.

Reinheit & Dokumentation

Handling Instructions (2659 KB)

Verweise

[1]. Decker MW, et al. Erysodine, a competitive antagonist at neuronal nicotinic acetylcholine receptors. European journal of pharmacology. 1995 Jun 23;280(1):79-89.

[2]. KONIUSZY F, et al. Erythrina alkaloids; studies on the constitution of erysodine erysovine and erysopine. J Am Chem Soc. 1949 Mar;71(3):875-8.

[3]. Mansbach RS, et al. Effects of the competitive nicotinic antagonist erysodine on behavior occasioned or maintained by nicotine: comparison with mecamylamine. Psychopharmacology. 2000 Feb;148(3):234-42. [Content Brief]

[4]. Quiroz G, et al. Erysodine, a competitive antagonist at neuronal nicotinic acetylcholine receptors, decreases ethanol consumption in alcohol-preferring UChB rats. Behavioural brain research. 2018 Sep 03;349:169-176. [Content Brief]

Calculators

Molaritätsrechner

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Konzentration Konzentration

Volumen Volumen

Molecular Weight Molecular Weight

Verdünnungsrechner

Konzentration _{(Stammlösung)} × Volumen _{(Stammlösung)} = Konzentration _{(Ziellösung)} × Volumen _{(Ziellösung)}

Konzentration _{(Stammlösung)} Konzentration _{(Stammlösung)}

Volumen _{(Stammlösung)} Volumen _{(Stammlösung)}

Konzentration _{(Ziellösung)} Konzentration _{(Ziellösung)}

Volumen _{(Ziellösung)} Volumen _{(Ziellösung)}

Help & FAQs

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1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

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Erysodine