SR 142948A
Based on 1 publication(s) in Google Scholar
SR 142948A is a blood-brain barrier-permeable, orally active, selective, non-peptide Neurotensin Receptor antagonist. SR 142948A exhibits an IC50 of 4.0 nM at the NTS1 site. SR 142948A competitively antagonizes neurotensin-dependent neurotransmitter release and modulates neurotensin-related dopaminergic and serotonergic signaling, making it useful for research on neurobehavioral mechanisms associated with schizophrenia.
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- Purity : 99.0%
- CAS No.: 184162-21-8
- 화학식: C39H52ClN5O6
- 분자량:722.31
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보관:
4°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
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Biological Activity
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Chemical Information
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용액&용해도
- Protocol
- 순도&문서
- References
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Help & FAQs
Publications Citing Use of MedChemExpress (MCE) SR 142948A
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Biological Activity
제품 설명
IC50 & Target
[1]|
Rat NTS1 4 nM (IC50) |
In Vitro
SR 142948A (60 min) displaces [3H]SR 142948A in a concentration-dependent manner in rat brain membrane homogenate competitive binding assays, with a Ki of 5.0 nM[1].
SR 142948A (60 min; 10 μM Levocabastine (HY-14277)) exhibits an IC50 of 4.0 nM for Levocabastine-insensitive NTS1 sites in rat brain membrane homogenates, whereas the IC50 is 7.0 nM for total NT1+NT2 sites in the absence of Levocabastine[1].
SR 142948A (3-100 nM) concentration-dependently right-shifts the neurotensin concentration-response curve in rat frontal cortex slices, with an apparent pA2 of 8.3; at 30 nM, it reduces the maximal effect of 1 μM neurotensin by 24%, and in a classical inhibition curve, it exhibits an IC50 of 4.5 nM against 100 nM neurotensin-induced K+-evoked [3H]5-HT release[2].
SR 142948A (3-100 nM) alone does not alter spontaneous or K+-evoked [3H]5-HT release in rat frontal cortex slices[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
SR 142948A (0.03-0.1 mg/kg; i.p.; single administration) does not alter spontaneous locomotor activity or psychostimulant-induced hyperactivity in male CD1 mice[4].
SR 142948A (0.03-0.1 mg/kg; i.p.; single administration; 10 min before Haloperidol (HY-14538) administration) attenuates 0.01 mg/kg Haloperidol-induced hypoactivity in male CD1 mice; 0.03 and 0.05 mg/kg are effective, with 0.05 mg/kg restoring locomotor activity to vehicle control levels, whereas 0.1 mg/kg shows no clear reversal effect[4].
SR 142948A (0.03-0.1 mg/kg; i.p.; single administration; combined with 0.04 mg/kg Haloperidol and psychostimulant challenge) attenuates the suppression of psychostimulant-induced hyperactivity by Haloperidol, with 0.03 and 0.05 mg/kg being effective but not fully reversing the effect of Haloperidol[4].
SR 142948A (0.03-0.1 mg/kg; i.p.; single administration; 10 min before Haloperidol administration) enhances 0.3 mg/kg Haloperidol-induced catalepsy, with 0.05 and 0.1 mg/kg being effective, whereas 0.03 mg/kg shows no clear effect[4].
SR 142948A (10 μg/kg; i.p.; single administration; 1 h before pre-exposure and conditioning) abolishes LI in male Sprague-Dawley rats receiving 0, 10, 20, or 40 stimulus pre-exposures; the vehicle control group still exhibits LI after 20 and 40 pre-exposures, whereas the SR 142948A group exhibits no LI at any pre-exposure level[5].
SR 142948A (0.25-1 mg/kg; i.p.; single administration; 20 min before psychostimulant challenge) inhibits psychostimulant-induced hyperactivity in male CD1 mice; both 0.25 and 1 mg/kg reduce locomotor activity during the 10-60 min observation period, with 1 mg/kg completely blocking hyperactivity; 1 mg/kg alone does not alter locomotor activity[6].
SR 142948A (1 mg/kg; i.p.; administered on days 1, 3, and 5; 20 min before conditioned stimulus) does not affect the formation of conditioned place preference (CPP) in male CD1 mice[6].
SR 142948A (0.1 mg/kg; i.p.; single administration) does not alter electrically stimulated dopamine efflux or basal tonic dopamine efflux in the nucleus accumbens or striatum of anesthetized male Sprague-Dawley rats[7].
SR 142948A (0.01-0.1 mg/kg; i.p.; single administration; 5 min before Haloperidol 50 μg/kg administration) enhances Haloperidol-promoted phasic electrical stimulation-induced dopamine efflux in the nucleus accumbens; Haloperidol alone increases the maximal effect by 51% compared with pre-administration, and the combination with 0.1 mg/kg SR 142948A increases it by 236%, while 0.01 mg/kg SR 142948A increases the effect by 97% at 30 min after Haloperidol administration; no clear enhancement is observed in the striatum[7].
SR 142948A (0.1 mg/kg; i.p.; single administration; 5 min before dopaminergic pharmacological stimulation) does not significantly alter the changes in nucleus accumbens dopamine efflux induced by high-dose Haloperidol, excitatory drugs, or Nomifensine (HY-B1110), but attenuates the decrease in dopamine efflux induced by dopamine receptor agonists, reducing the maximum decrease from 55% to 30% and shortening the duration of the decrease[7].
SR 142948A (10-100 μg/kg; i.p.; single administration; 1 h before antipsychotic administration) region-selectively modulates antipsychotic-induced Fos expression in male Sprague-Dawley rats: no significant effect in the medial prefrontal cortex, nucleus accumbens shell, and lateral septum; increases olanzapine-induced Fos-positive neurons by 38% and 57% in the dorsomedial caudate putamen; decreases haloperidol-induced Fos expression by 37% and 29% and increases olanzapine-induced Fos-positive neurons by 35% and 135% in the dorsolateral caudate putamen[8].
SR 142948A (100 μg/kg; i.p.; single administration; 1 h before antipsychotic administration) alone does not induce significant catalepsy and does not significantly alter Haloperidol- or Clozapine (HY-14539)-related catalepsy in either the block test or the bar test; when combined with Olanzapine (HY-14541), it enhances catalepsy, with enhancement at 15 and 30 min in the block test and increased catalepsy scores at 5, 15, and 60 min in the bar test[8].
SR 142948A (0.1-10 μM; 65 nL local administration into the ventral tegmental area; single administration; 1 min before 0.1 μM Neurotensin administration) dose-dependently inhibits neurotensin-induced dopamine efflux in the nucleus accumbens of anesthetized male Sprague-Dawley rats pretreated with pargyline; 3 and 10 μM reduce the effect by 53% and 81%, respectively, while 0.1 and 1 μM show no significant effect, and the inhibitory effects of 3 and 10 μM remain at 38% and 47%, respectively, at 16 min[9].
SR 142948A (0.1-100 μg/kg; i.p.; single administration; 1 h before pre-exposure and conditioning) dose-dependently disrupts latent inhibition (LI) in male Sprague-Dawley rats; with 20 stimulus pre-exposures, the 0.1 and 1 μg/kg groups still retain LI, whereas the 10 and 100 μg/kg groups no longer exhibit LI; with 30 stimulus pre-exposures, none of the tested dose groups exhibit LI. None of the doses significantly affect conditioned response inhibition in non-pre-exposed rats[5].
SR 142948A (10 μg/kg; i.p.; single administration; 1 h before pre-exposure and conditioning; Sulpiride (HY-B1019) 100 mg/kg i.p. administered 30 min before the experiment) alone disrupts 30 pre-exposure-induced LI, whereas LI is restored when combined with the dopamine D2 receptor antagonist Sulpiride; no significant treatment effect is observed in the non-pre-exposed group[5].
SR 142948A (0.003-0.1 mg/kg; i.p.; single administration; 5 min before Haloperidol 50 μg/kg administration) dose-dependently enhances Haloperidol-induced sustained dopamine efflux in the nucleus accumbens; Haloperidol alone increases the maximal effect by 137%, and combined with 0.1 mg/kg SR 142948A it increases by 228%, while 0.003 mg/kg has no effect and 0.01 mg/kg shows a trend toward enhancement[7].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:CD-1 (Male, 22-24 g)[6]
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Dosage:0.25 mg/kg; 1 mg/kg
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Administration:i.p.; 20 min before MDMA
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Result:Reduced hyperlocomotion throughout 10-60 min at both doses.
Completely blocked hyperlocomotion at 1 mg/kg.
Did not alter locomotor activity when administered alone at 1 mg/kg.
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Animal Model:CD-1 (Male, 22-24 g)[6]
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Dosage:1 mg/kg
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Administration:i.p.; 20 min before MDMA; days 1, 3 and 5
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Result:No significant effect on the acquisition of MDMA-induced CPP.
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Animal Model:CD-1 (Male, 22-24 g)[6]
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Dosage:1 mg/kg
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Administration:i.p.; single dose on test day
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Result:Blocked expression of conditioned place preference.
Did not reduce total compartment entries.
Did not reduce total distance traveled.
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Animal Model:Long-Evans (female, 250-275 g, intact cycling)[3]
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Dosage:0.1 mg/kg
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Administration:i.p.; single injection; 1 h before PPI testing
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Result:Significantly decreased PPI during D1 and P at 13:00 h.
Significantly decreased PPI during P at 01:00 h.
Significantly increased PPI during D1 at 01:00 h.
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Animal Model:CD1 (male, 25-35 g)[4]
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Dosage:0.03 mg/kg; 0.05 mg/kg; 0.1 mg/kg
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Administration:i.p.; single dose; 10 min before Haloperidol
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Result:Attenuated haloperidol-induced hypolocomotion at 0.03 and 0.05 mg/kg.
Restored locomotor activity to the vehicle level at 0.05 mg/kg.
Showed no clear reversal at 0.1 mg/kg.
ncreased catalepsy at 0.05 and 0.1 mg/kg.
Showed no clear effect at 0.03 mg/kg.
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Animal Model:Sprague-Dawley rats (adult male, 250-300 g)[5]
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Dosage:0.1, 1.0, 10, 100 µg/kg
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Administration:i.p.; single dose; 1 h before pre-exposure and conditioning
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Result:Retained LI at 0.1 and 1 μg/kg after 20 pre-exposures.
Abolished LI at 10 and 100 μg/kg after 20 pre-exposures.
Abolished LI at all tested doses after 30 pre-exposures.
Did not alter conditioned response suppression in non-pre-exposed animals.
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Animal Model:Sprague-Dawley rats (adult male, 250-300 g)[5]
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Dosage:10 μg/kg
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Administration:i.p.; single administration; 1 h prior to pre-exposure and conditioning
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Result:Abolished LI at all pre-exposure levels.
Vehicle controls retained LI after 20 and 40 pre-exposures.
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Animal Model:Sprague-Dawley rats (adult male, 250-300 g)[5]
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Dosage:10 µg/kg
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Administration:i.p.; single dose; ±Sulpiride
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Result:Disrupted LI when administered alone.
LI was restored by sulpiride coadministration.
Did not produce a treatment effect in non-pre-exposed rats.
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Animal Model:Sprague-Dawley rats (adult male, 300-400 g)[8]
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Dosage:10, 100 μg/kg
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Administration:i.p.; single dose; 1 h before antipsychotic drug
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Result:Did not clearly alter Fos expression in the PFC, NAcc shell or lateral septum.
Increased olanzapine-induced Fos-positive neurons by 38% and 57% in the dorsomedial CPu.
Decreased haloperidol-induced Fos expression by 37% and 29% in the dorsolateral CPu.
Increased olanzapine-induced Fos-positive neurons by 35% and 135% in the dorsolateral CPu.
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Animal Model:Sprague-Dawley rats (adult male)[8]
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Dosage:100 μg/kg
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Administration:i.p.; single dose; 1 h before antipsychotic drug
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Result:Did not produce marked catalepsy alone.
Did not clearly alter haloperidol- or clozapine-associated catalepsy.
Enhanced olanzapine-associated cataleptic behavior in both assays.
Chemical Information
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CAS No. 184162-21-8
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Appearance Solid
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분자량 722.31
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화학식 C39H52ClN5O6
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Color White to off-white
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SMILES
O=C(C1(NC(C2=NN(C3=CC=C(C(N(CCCN(C)C)C)=O)C=C3C(C)C)C(C4=C(OC)C=CC=C4OC)=C2)=O)C5CC6CC(C5)CC1C6)O.Cl
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선적
Room temperature in continental US; may vary elsewhere.
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보관
4°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Publications (1)
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Journal Impact Factor
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Most Recent
용액&용해도
In Vitro:
H2O : 10 mg/mL (13.84 mM; Need ultrasonic and warming)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
* 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. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
* 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)
Protocol
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
순도&문서
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Data Sheet (305 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
[1]. Betancur C, et al. Characterization of binding sites of a new neurotensin receptor antagonist, [3H]SR 142948A, in the rat brain. Eur J Pharmacol. 1998;343:67-77. [Content Brief]
[9]. Leonetti M, et al. The neurotensin receptor antagonist SR 142948A blocks the efflux of dopamine evoked in nucleus accumbens by neurotensin ejection into the ventral tegmental area. Naunyn-Schmiedeberg's archives of pharmacology. 2002 Jun;365(6):427-33. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| H2O | 1 mM | 1.3844 mL | 6.9222 mL | 13.8445 mL | 34.6112 mL |
| 5 mM | 0.2769 mL | 1.3844 mL | 2.7689 mL | 6.9222 mL | |
| 10 mM | 0.1384 mL | 0.6922 mL | 1.3844 mL | 3.4611 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.
SR 142948A Related Classifications
HY-124767 Related Classifications
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Keywords
- SR 142948A
- 184162-21-8
- Neuropeptide Y Receptor
- nucleus accumbens
- latent inhibition
- rat brain membranes
- levocabastine-insensitive neurotensin NT1 receptors
- mesolimbic dopamine efflux
- schizophrenia
- prepulse inhibition of the acoustic startle reflex
- ventral tegmental area
- neurotensin receptor antagonist
- levocabastine-sensitive neurotensin NT2 receptors
- Inhibitor
- inhibitor
- inhibit