RB 101
RB 101 is a blood-brain barrier-crossing prodrug as well as aminopeptidase N and neutral endopeptidase-24.11 inhibitor. RB 101 blocks enkephalin breakdown, elevates extracellular enkephalin levels and activate δ-opioid receptor and dopamine D1 receptor. RB 101 can be used for the research of pain, depressive syndromes, and diabetic neuropathy.
For research use only. We do not sell to patients.
- CAS No.: 135949-60-9
- Formula: C31H38N2O3S3
- Molecular Weight:582.84
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Storage:
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
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
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δ Opioid Receptor/DOR |
D1 Receptor |
RB 101 (5-20 mg/kg; i.v.; single administration) potentiates stress-induced analgesia in mice, reaching 85% analgesia at 5 mg/kg when combined with warm-water swim stress[1].
RB 101 (1.25-10 mg/kg; i.v.; single slow injection) induces a dose-dependent, long-lasting increase in spontaneous motor activity in mice via δ opioid and dopamine D1 receptor stimulation[2].
RB 101 (2.5-10 mg/kg; i.v.; single slow injection) dose-dependently attenuates conditioned suppression of motility in shocked mice and increases striatal dopamine turnover, via δ opioid and dopamine D1 receptor stimulation[2].
RB 101 (2.5-10 mg/kg; i.v.; single slow injection (20 s); 10 min before testing) significantly reduces immobility time in the mouse forced swim test via δ opioid and dopamine D1 receptor stimulation[2].
RB 101 (5-40 mg/kg; i.v.) produces dose-dependent, μ- and δ-opioid receptor-mediated antinociception in Streptozocin (HY-13753)-induced diabetic rats with neuropathic pain, completely suppressing mechanical hyperalgesia at doses of 20 and 40 mg/kg i.v.[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Male albino mice (Depre, France; 20-22 g)[1]
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Dosage:2.5 mg/kg; 5 mg/kg; 10 mg/kg; 20 mg/kg; 40 mg/kg
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Administration:i.v.; single administration
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Result:Induced a dose-dependent reduction in [3H]diprenorphine binding: 5 mg/kg caused 20% displacement, 10 mg/kg caused 30% displacement (plateau effect), with no additional displacement at 20 mg/kg.
Induced a non-significant increase in jump latency at 5 mg/kg.
Produced statistically significant analgesia relative to controls at 10 mg/kg, 20 mg/kg, and 40 mg/kg, with analgesia percentages increasing with dose.
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Animal Model:Male albino mice (Depre, France; 20-22 g; forced warm-water swim stress model)[1]
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Dosage:5 mg/kg; 20 mg/kg
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Administration:i.v.; single administration
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Result:Combined with stress induced 85% analgesia at 5 mg/kg (vs. 48% analgesia from stress alone), and this combined analgesia was blocked by naloxone but not by naltrindole.
Combined with stress caused 45% displacement of [3H]diprenorphine relative to unstressed controls at 5 mg/kg, while 20 mg/kg combined with stress caused 43% displacement relative to unstressed controls.
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Animal Model:Swiss albino mice (male, 20-22 g for spontaneous motor activity and forced swim tests; ~30 g, 8 weeks old for conditioned suppression of motility test)[2]
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Dosage:1.25 mg/kg; 2.5 mg/kg; 5 mg/kg; 10 mg/kg
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Administration:i.v.; single slow injection
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Result:Induced a dose-dependent increase in locomotor activity, with effects peaking between 5-10 min post-injection.
Remained significant at 15 and 20 min post-injection at 10 mg/kg.
Produced a significant cumulative increase in motor activity (linear locomotion + rears) over 10 and 20 min at 5 mg/kg, which was antagonized by pre-treatment with naltrindole (0.1 mg/kg s.c.) and SCH 23390 (0.07 mg/kg s.c.), but not sulpiride (25 mg/kg i.p.).
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Animal Model:Swiss albino mice (male, ~30 g, 8 weeks old)[2]
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Dosage:2.5 mg/kg; 5 mg/kg; 10 mg/kg
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Administration:i.v.; single slow injection
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Result:Did not alter locomotor activity at 2.5 and 5 mg/kg, but increased activity at 10 mg/kg in non-shocked mice.
Dose-dependently reduced conditioned motility suppression at 5 and 10 mg/kg in shocked mice.
Effect of 5 mg/kg was antagonized by pre-treatment with naltrindole (0.1 mg/kg s.c.) and SCH 23390 (0.07 mg/kg s.c.), but not sulpiride (25 mg/kg i.p.).
Significantly increased striatal DOPAC/DA and HVA/DA ratios to 0.108 and 0.100, respectively, in shocked mice treated with 5 mg/kg, an effect blocked by naltrindole.
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Animal Model:Swiss albino mice (male, 20-22 g)[2]
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Dosage:2.5 mg/kg; 5 mg/kg; 10 mg/kg
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Administration:i.v.; single slow injection
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Result:Significantly shortened the duration of immobility in the forced swim test at 5 and 10 mg/kg.
Effect of 5 mg/kg was antagonized by pre-treatment with naltrindole (0.1 mg/kg s.c.) and SCH 23390 (0.07 mg/kg s.c.), but not sulpiride (25 mg/kg i.p.).
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Animal Model:Sprague-Dawley (male, 300 g, Streptozocin-induced neuropathic pain)[3]
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Dosage:5 mg/kg; 10 mg/kg; 20 mg/kg; 40 mg/kg
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Administration:i.v.
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Result:Produced a dose-dependent antinociceptive effect on mechanical hyperalgesia, with 20 and 40 mg/kg doses completely suppressing diabetes-induced hyperalgesia (P<0.001).
Achieved a maximal vocalization threshold elevation of +294 g (+178% of predrug score) at 20 minutes with 40 mg/kg dose, which was not significantly different from the maximal effect of 20 mg/kg.
Had a short duration of action (20 minutes) with 5 mg/kg dose, while 10, 20, and 40 mg/kg doses lasted 60 minutes.
Showed a ceiling effect at 40 mg/kg confirmed by AUC values.
Produced a significant increase in withdrawal threshold for mechanical allodynia only with 40 mg/kg dose, with a maximal increase of +8.3 g at 20 minutes (P<0.01), lasting 20 minutes.
Did not significantly affect tail immersion reaction time for thermal allodynia at any dose.
Had its antinociceptive effect at 20 mg/kg completely abolished by pretreatment with 0.5 mg/kg i.v. naloxone or 1 μg/rat i.t. naltrindole.
Chemical Information
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CAS No. 135949-60-9
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Molecular Weight 582.84
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Formula C31H38N2O3S3
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SMILES
CSCC[C@H](N)CSSCC(CC1=CC=CC=C1)C(N[C@H](C(OCC2=CC=CC=C2)=O)CC3=CC=CC=C3)=O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
[1]. Ruiz-Gayo M, et al. In vivo occupation of mouse brain opioid receptors by endogenous enkephalins: blockade of enkephalin degrading enzymes by RB 101 inhibits [3H]diprenorphine binding. Brain Res. 1992;571(2):306-312. [Content Brief]
[2]. Baamonde A, et al. Antidepressant-type effects of endogenous enkephalins protected by systemic RB 101 are mediated by opioid delta and dopamine D1 receptor stimulation. Eur J Pharmacol. 1992;216(2):157-166. [Content Brief]
[3]. Coudoré-Civiale MA, et al. Enhancement of the effects of a complete inhibitor of enkephalin-catabolizing enzymes, RB 101, by a cholecystokinin-B receptor antagonist in diabetic rats. Br J Pharmacol. 2001;133(1):179-185. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
RB 101 Related Classifications
HY-117702 Related Classifications
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- RB 101
- 135949-60-9
- RB101
- RB-101
- Prolyl Endopeptidase (PREP)
- Aminopeptidase
- Opioid Receptor
- Dopamine Receptor
- Drug Intermediate
- streptozocin-induced diabetic rats
- rat spinal cord tissue
- aminopeptidase N
- neutral endopeptidase-24.11
- μ-opioid receptors
- mouse brain
- diabetic neuropathy
- dopamine D1 receptors
- δ opioid receptors
- enkephalin
- Inhibitor
- inhibitor
- inhibit