TAT-D1 peptide acetate
Based on 1 Customer Validation
TAT-D1 peptide acetate is a dopamine D1-D2 receptor heterodimer inhibitor. TAT-D1 peptide acetate disrupts the function of dopamine D1-D2 receptor heteromers, enhances subchronic amphetamine-induced locomotor activity, and exacerbates the expression of amphetamine-induced locomotor sensitization. TAT-D1 peptide acetate produces rapid anxiolytic and antidepressant-like effects in rat models of depression and anxiety, and inhibits c-fos expression in the nucleus accumbens of rats. TAT-D1 peptide acetate can be used in the research of psychostimulant addiction, depression and anxiety disorders.
For research use only. We do not sell to patients.
- Formula: C144H257N57O43·xC2H4O2
- Molecular Weight:3474.94 (free base)
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Storage:
Sealed storage, away from moisture.
Powder -80°C, 2 years , -20°C, 1 year* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
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
- Purity & Documentation
- References
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Help & FAQs
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Biological Activity
TAT-D1 peptide (i.c.v.; single dose, 300 pM) acetate exerts antidepressant-like effects in unstressed rats by reducing the total immobility time in the forced swim test; it exerts anxiolytic-like effects by increasing the time rats spend in the open arms of the elevated plus maze and shortening the feeding latency in the novelty-suppressed feeding test. It exerts rapid antidepressant effects by reversing the anhedonic reduction in sucrose preference in rats exposed to chronic unpredictable stress (CUS), completely reversing the CUS-induced prolongation of feeding latency in a novel environment, and increasing the intake of Froot Loops. It inhibits SKF 83959 (HY-130344)-induced c-fos expression in the nucleus accumbens and SKF 83959-induced grooming behavior, while administration alone induces region-specific c-fos expression in the cortex, anterior olfactory area, lateral habenula and thalamus[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Sprague-Dawley (adult male, 300-350 g)[1]
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Dosage:300 pM (acute pre-administration; co-administration; repeated administration)
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Administration:intracerebroventricular (i.c.v.); 15 minutes prior to injection; daily for 5 consecutive days; single dose
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Result:Elevated total 60-minute locomotor activity to 2918.1 beam breaks, a significant increase compared to saline controls.
Induced a robust locomotor increase in the first 5 minutes post-injection that was significantly higher than controls.
Did not produce a significant change in locomotor activity in non-habituated rats compared to vehicle controls.
Significantly enhanced locomotor responsiveness to amphetamine across the 5-day regimen compared to amphetamine alone (p < 0.05).
Induced a sensitized locomotor response to the priming amphetamine injection with total 60-minute activity of 7337.0 ± 920.4 beam breaks, significantly higher than saline-pretreated controls and comparable to amphetamine-sensitized rats.
Further enhanced the sensitized locomotor response to the priming amphetamine injection with total 60-minute activity of 8989.3 beam breaks, significantly higher than both saline-pretreated controls and amphetamine-sensitized rats .
Did not alter the expression of locomotor sensitization in amphetamine-sensitized rats, with total 60-minute activity of 7948.5 beam breaks, significantly higher than saline-pretreated controls.
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Animal Model:Sprague-Dawley (adult male, 300-400 g); Fischer 344 (adult male, 300-400 g, chronic unpredictable stress model)[2]
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Dosage:300 pM
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Administration:i.c.v.; single dose
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Result:Significantly reduced total immobility timein forced swim test.
Significantly increased time spent in open arms per entryand reduced total open arm entriesin elevated plus maze.
Significantly reduced latency to drink milk in novel environment in novelty-induced hypophagia test.
Abolished SKF 83959-induced reduction in latency to immobility and increase in immobility within first minute of forced swim test.
Abolished SKF 83959-induced reduction in time spent in open arms per entry and total time spent in open arms in elevated plus maze.
Robustly attenuated SKF 83959-induced enhanced latency to drink milk and reinstated total milk consumption in novelty-induced hypophagia test.
Partially reversed CUS-induced reduction in sucrose preference scores, eliminating significant difference between CUS-exposed and non-exposed control rats.
Completely reversed CUS-induced increase in latency to consume fruit loops to non-stressed control levels; significantly increased total fruit loops consumed in CUS-exposed and non-exposed control rats.
Completely abolished CUS-induced prolongation of feeding latency in novel environment, restoring latency to non-stressed control levels.
Showed no significant effect on total time spent in open arms in elevated plus maze.
Significantly reduced SKF 83959-induced c-fos expression in nucleus accumbens (NAc) core and NAc shell.
Abolished SKF 83959-induced grooming behavior, reducing grooming time.
Induced significant c-fos expression in multiple brain regions when administered standalone: anterior olfactory nucleus, orbitofrontal cortex, infralimbic cortex, prelimbic cortex, piriform cortex, lateral habenula, thalamic nuclei.
Showed no effect on c-fos expression in striatal subregions, ventral pallidum, globus pallidus, lateral hypothalamus, hippocampus, amygdala, substantia nigra, ventral tegmental area, or rostromedial tegmental nucleus when administered standalone.
Chemical Information
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Appearance Solid
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Molecular Weight 3474.94 (free base)
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Formula C144H257N57O43·xC2H4O2
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SMILES
O=C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CCCCN)C(N[C@@H](CCCCN)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CCC(N)=O)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CCCNC(N)=N)C(N1[C@@H](CCC1)C(N[C@@H](CCC(N)=O)C(NCC(N[C@@H](CO)C(N[C@@H](CO)C(N[C@@H](CCC(O)=O)C(N[C@@H](CC(O)=O)C(N[C@@H](CC(C)C)C(N[C@@H](CCCCN)C(N[C@@H](CCCCN)C(N[C@@H](CCC(O)=O)C(N[C@@H](CCC(O)=O)C(N[C@@H](C)C(N[C@@H](C)C(NCC(N[C@@H]([C@@H](C)CC)C(N[C@@H](C)C(N[C@@H](CCCNC(N)=N)C(N2[C@@H](CCC2)C(N[C@@H](CC(C)C)C(O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)CN.CC(O)=O.[x]
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Sequence
Gly-Arg-Lys-Lys-Arg-Arg-Gln-Arg-Arg-Arg-Pro-Gln-Gly-Ser-Ser-Glu-Asp-Leu-Lys-Lys-Glu-Glu-Ala-Ala-Gly-Ile-Ala-Arg-Pro-Leu
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Sequence Shortening
GRKKRRQRRRPQGSSEDLKKEEAAGIARPL
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Sealed storage, away from moisture
Powder -80°C 2 years -20°C 1 year * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Solvent & Solubility
H2O : ≥ 100 mg/mL
* "≥" means soluble, but saturation unknown.
Purity & Documentation
References
[1]. Shen MY, et al. The dopamine D1-D2 receptor heteromer exerts a tonic inhibitory effect on the expression of amphetamine-induced locomotor sensitization. Pharmacol Biochem Behav. 2015;128:33-40. [Content Brief]
[2]. Shen MY, et al. Rapid anti-depressant and anxiolytic actions following dopamine D1-D2 receptor heteromer inactivation. Eur Neuropsychopharmacol. 2015;25(12):2437-2448. [Content Brief]
[3]. Perreault ML, et al. Regulation of c-fos expression by the dopamine D1-D2 receptor heteromer. Neuroscience. 2015;285:194-203. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
TAT-D1 peptide acetate Related Classifications
HY-P10405A Related Classifications
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