CTDP-32476
CTDP-32476 is a dopamine transporter (DAT) inhibitor with a Ki value of 12 nM for human DAT, and exhibits moderate affinity for norepinephrine transporter (NET). CTDP-32476 blocks DAT to increase extracellular dopamine levels, induces motor enhancement and brain stimulation reward effects in rats, inhibits self-administration behavior and cue-induced relapse behavior, and shows no reinforcing activity with low addiction potential. CTDP-32476 can be used in studies related to addiction to tropane alkaloid psychostimulants.
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- CAS No.: 928046-68-8
- 화학식: C16H25Cl2N
- 분자량:302.28
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
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
- 순도&문서
- References
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Help & FAQs
Biological Activity
CTDP-32476 (10 nM-100 μM; 60 min) potently binds to human DAT expressed in HEK293 cells, with a Ki value of 12 nM[1].
CTDP-32476 (10 pM-100 μM; 60 min) is a potent competitive inhibitor of human DAT expressed in HEK293 cells, which inhibits the binding of [3H]-cocaine to DAT, with a Ki value of 0.12 nM at the high-affinity site and 123 nM at the low-affinity site[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
CTDP-32476 (0.5 mg/kg; intravenous injection; administered daily for 3 hours for 7 consecutive days) fails to maintain the schedule-controlled intravenous self-administration behavior in rats trained to self-administer a Schedule II psychostimulant[1].
The rewarding efficacy of CTDP-32476 (0.25-1.0 mg/kg; intravenous injection; administered daily for 3 consecutive days) is significantly lower than that of psychostimulants[1].
CTDP-32476 (3-20 mg/kg; i.p.; single administration) dose-dependently suppresses schedule-controlled self-administration behavior under a fixed ratio 2 reinforcement schedule in rats with a history of stimulant exposure[1].
Pretreatment with CTDP-32476 (3-20 mg/kg; intraperitoneal injection; single administration) reduces the rewarding efficacy of psychostimulants, with a significant effect observed at the dose of 20 mg/kg[1].
Pretreatment with CTDP-32476 (10-20 mg/kg; intraperitoneal injection; single administration) dose-dependently reduces psychostimulant self-administration behavior and total intake in rats with a history of psychostimulant exposure within a certain dose range[1].
Chronic daily administration of CTDP-32476 (10-20 mg/kg; i.p.; once daily for 7 consecutive days) during extinction training significantly reduces cue-induced relapse of controlled stimulant-seeking behavior in rats with a history of controlled stimulant exposure[1].
Systemic administration of CTDP-32476 (10-20 mg/kg; i.p.; single dose) slowly induces a persistent increase in dopamine (DA) levels in the nucleus accumbens, and both systemic administration and local perfusion of CTDP-32476 (30 μM; local perfusion in the nucleus accumbens; single dose) attenuate the cocaine-induced elevation of extracellular DA levels in the nucleus accumbens[1].
Systemic administration of CTDP-32476 (3-10 mg/kg; i.p.; single dose) induces slow-onset, long-lasting, dose-dependent enhancement of spontaneous activity in rats, an effect that differs from the rapid-onset action of cocaine[1].
Systemic administration of CTDP-32476 (3-10 mg/kg; i.p.; single dose) produces a slow-onset, long-lasting, and dose-dependent enhancement of brain stimulation reward in rats, which differs from the rapid-onset effect of cocaine[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Long-Evans (male, initial weight 250-300 g, drug-naive, trained for intravenous self-administration under fixed-ratio 2 reinforcement)[1]
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Dosage:0.5, 1.0 mg/kg
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Administration:i.v.; 3-hour sessions for 10 days
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Result:Did not acquire stable self-administration at either dose.
Revealed a statistically significant treatment main effect, with no significant difference between saline and CTDP-32476 groups.
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Animal Model:Long-Evans (male, initial weight 250-300 g, schedule-controlled intravenous self-administration-trained, tested for substitution under fixed-ratio 2 reinforcement)[1]
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Dosage:0.5 mg/kg
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Administration:i.v.; 3-hour sessions for 7 days
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Result:Did not sustain stable self-administration.
Revealed a statistically significant treatment main effect and time main effect.
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Animal Model:Long-Evans (male, initial weight 250-300 g, psychostimulant self-administration-trained, tested for substitution under progressive-ratio reinforcement)[1]
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Dosage:0.25, 0.5, 1.0 mg/kg
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Administration:i.v.; daily sessions for 3 days
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Result:Produced significantly lower progressive-ratio break points than equivalent doses of psychostimulant at 0.5 mg/kg and 1.0 mg/kg/infusion.
Showed a progressive reduction in break points over the 3 sessions of CTDP-32476 substitution.
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Animal Model:Long-Evans (male, initial weight 250-300 g, schedule-controlled self-administration-trained, tested for pretreatment effects under fixed-ratio 2 reinforcement)[1]
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Dosage:3, 10, 20 mg/kg
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Administration:i.p.; single dose
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Result:Dose-dependently inhibited schedule-controlled self-administration with 10 mg/kg and 20 mg/kg producing statistically significant reductions in target infusions relative to vehicle controls.
Showed no effect on inactive lever responding.
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Animal Model:Long-Evans (male, initial weight 250-300 g, psychostimulant self-administration-trained, tested for pretreatment effects under progressive-ratio reinforcement)[1]
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Dosage:3, 10, 20 mg/kg
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Administration:i.p.; single dose
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Result:Dose-dependently lowered the progressive-ratio break point for psychostimulant self-administration, with 20 mg/kg producing a statistically significant reduction relative to vehicle controls.
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Animal Model:Long-Evans (male, initial weight 250-300 g, psychostimulant self-administration-trained, tested for pretreatment effects on multiple-dose psychostimulant self-administration)[1]
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Dosage:10, 20 mg/kg
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Administration:i.p.; single dose
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Result:Dose-dependently shifted the psychostimulant self-administration dose-response curve downward and shifted the psychostimulant intake dose-response curve downward and to the right, with significant reductions in infusions and intake across all tested psychostimulant doses relative to vehicle controls.
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Animal Model:Long-Evans (male, initial weight 250-300 g, controlled stimulant self-administration-trained, extinguished controlled stimulant-seeking, tested for cue-induced reinstatement after chronic pretreatment)[1]
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Dosage:10, 20 mg/kg
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Administration:i.p.; once daily for 7 days
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Result:Significantly attenuated cue-induced reinstatement of drug-seeking behavior, while a single pretreatment dose did not alter controlled stimulant-primed reinstatement.
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Animal Model:Long-Evans (male, initial weight 250-300 g, with in vivo brain microdialysis probes in the nucleus accumbens)[1]
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Dosage:10, 20, 30 mg/kg
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Administration:i.p.; single dose
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Result:Produced a slow-onset (20-60 min), long-duration (6-12 h) dose-dependent increase in extracellular nucleus accumbens dopamine (DA).
Pretreatment with 10 mg/kg and 20 mg/kg significantly attenuated cocaine-enhanced extracellular DA.
Local intra-nucleus accumbens perfusion of 30 μM blocked cocaine-enhanced extracellular DA.
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Animal Model:Long-Evans (male, initial weight 250-300 g, drug-naive, tested for locomotor activity)[1]
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Dosage:3, 10 mg/kg
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Administration:i.p.; single dose
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Result:Produced a slow-onset (20-60 min), long-duration (6 h) dose-dependent increase in locomotor activity, which was significantly different from the fast-onset, short-duration effect of cocaine.
Revealed a statistically significant treatment main effect and time main effect.
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Animal Model:Long-Evans (male, initial weight 250-300 g, implanted with medial forebrain bundle electrodes, trained for brain-stimulation reward)[1]
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Dosage:3, 10 mg/kg
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Administration:i.p.; single dose
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Result:Produced a slow-onset (20-60 min), long-duration (up to 9 h) dose-dependent decrease in brain-stimulation reward thresholds.
Revealed a statistically significant treatment main effect and time main effect.
Chemical Information
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CAS No. 928046-68-8
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분자량 302.28
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화학식 C16H25Cl2N
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SMILES
[C@@H](CC(C)C)(C1=CC=C(Cl)C=C1)[C@]2(CCCCN2)[H].Cl
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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