RU 24969CAS# 66611-26-5 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 66611-26-5 | SDF | Download SDF |
| PubChem ID | 108029 | Appearance | Powder |
| Formula | C14H16N2O | M.Wt | 228.29 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Solubility | DMSO : ≥ 30 mg/mL (131.41 mM) *"≥" means soluble, but saturation unknown. | ||
| Chemical Name | 5-methoxy-3-(1,2,3,6-tetrahydropyridin-4-yl)-1H-indole | ||
| SMILES | COC1=CC2=C(C=C1)NC=C2C3=CCNCC3 | ||
| Standard InChIKey | KRVMLPUDAOWOGN-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C14H16N2O/c1-17-11-2-3-14-12(8-11)13(9-16-14)10-4-6-15-7-5-10/h2-4,8-9,15-16H,5-7H2,1H3 | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
RU 24969 Dilution Calculator
RU 24969 Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 4.3804 mL | 21.902 mL | 43.8039 mL | 87.6079 mL | 109.5098 mL |
| 5 mM | 0.8761 mL | 4.3804 mL | 8.7608 mL | 17.5216 mL | 21.902 mL |
| 10 mM | 0.438 mL | 2.1902 mL | 4.3804 mL | 8.7608 mL | 10.951 mL |
| 50 mM | 0.0876 mL | 0.438 mL | 0.8761 mL | 1.7522 mL | 2.1902 mL |
| 100 mM | 0.0438 mL | 0.219 mL | 0.438 mL | 0.8761 mL | 1.0951 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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RU 24969-produced adipsia and hyperlocomotion: differential role of 5HT 1A and 5HT 1B receptor mechanisms.[Pubmed:24844705]
Pharmacol Biochem Behav. 2014 Sep;124:1-4.
RU 24969 is a widely used, but non-selective, 5-HT1B/1A agonist that decreases fluid consumption and increases forward locomotion. The mechanism underlying these behavioural responses is not, however, well understood. Accordingly, effects of the selective 5-HT1A and 5-HT1B antagonists, WAY 100635, and GR 127935, respectively, on these two responses to RU 24969 were determined. RU 24969 (0.03-3.0mg/kg, s.c.) dose-dependently decreased water consumption in water deprived rats. This effect was attenuated by GR 127935 (3.0mg/kg), but not by WAY 100635 (1.0mg/kg). RU 24969 (0.3-3.0mg/kg) dose-dependently increased forward locomotion but a higher dose was required to produce this response than the adipsic response. The increased locomotor response was attenuated by WAY 100635 (1.0mg/kg), but not GR 127935 (3.0mg/kg). These results suggest that RU 24969-induced adipsia is mediated by 5-HT1B mechanisms, while RU 24969-induced hyperlocomotion is mediated by 5-HT1A mechanisms.
Subthalamic 5-HT(1A) and 5-HT(1B) receptor modulation of RU 24969-induced behavioral profile in rats.[Pubmed:11888548]
Pharmacol Biochem Behav. 2002 Apr;71(4):569-80.
The effects of systemic administration of the serotonin (5-HT)(1A/1B) agonist 5-methoxy-3-(1,2,3,6-tetrahydropyridin-4-yl)1H-indole (RU 24969) on locomotor and investigatory behavior in rats have been well characterized using the behavioral pattern monitor (BPM). To elucidate the neural circuitry underlying this behavioral profile, intracerebral dose--response studies were conducted at two sites with high densities of 5-HT(1B) receptors, the subthalamic nucleus (STN) and substantia nigra. Infusion of RU 24969 into the STN produced systemic RU 24969-like changes in locomotor activity and patterns but an uncharacteristic increase in investigatory holepokes. Intra-STN administration of the selective 5-HT(1A) receptor agonist 8-hydroxy-2-(di-N-propylamino)tetralin (8-OH-DPAT) produced RU 24969-like changes in locomotor patterns only, while the 5-HT(1B) receptor agonist 3(1,2,5,6-tetrahydropyrid-4-yl)pyrrolo[3,2-b]pyrid-5-one dihydrochloride (CP-93,129) increased locomotor activity, produced no change in locomotor patterns and nonsignificantly increased holepokes. Intranigral infusion of RU 24969 produced systemic and intra-STN RU 24969-like increases in locomotor activity. Intranigral RU 24969, however, failed to produce any changes in locomotor patterns or investigatory holepokes. Intranigral infusions of CP-93,129 or 8-OH-DPAT had no effects on locomotor activity, locomotor patterns or investigatory holepokes. These results provide evidence for multiple-site mediation of the locomotor-activating effects of RU 24969 and for a dissociation of the neural substrates underlying locomotor and investigatory components of the RU 24969-induced behavioral profile.
RU-24969 disrupts d-amphetamine self-administration and responding for conditioned reward via stimulation of 5-HT1B receptors.[Pubmed:10780831]
Behav Pharmacol. 1999 Mar;10(2):183-93.
Behavioural and neurochemical evidence indicates a facilitatory effect of 5-hydroxytryptamine (5-HT), acting via 5-HT1B receptors, on dopamine (DA) systems. To explore this interaction further, these experiments examined the effects of the 5-HT1A/1B agonist RU-24969 on behaviours known to involve the mesolimbic DA system. These behaviours were locomotor activity, intravenous self-administration of d-amphetamine, responding for a conditioned reward (CR), and the response potentiating effects of amphetamine on CR responding. Locomotor activity was enhanced by 1 and 3 mg/kg RU 24969, and both doses also reduced responding for d-amphetamine (60 microg/kg/infusion). Changing the unit dose produced a characteristic U-shaped dose-response curve. This dose-response relationship was not apparent following injection of RU-24969. Across all unit infusion doses of amphetamine, the level of responding was fairly constant. In the CR experiments, rats responded for a conditioned stimulus that was previously paired with water. RU-24969 completely disrupted responding for CR, and also abolished CR responding in rats injected with 3 microg d-amphetamine in the nucleus accumbens. RU-24969 also markedly suppressed responding for water. The suppressant actions of RU-24969 on amphetamine self-administration and CR responding involve stimulation of 5-HT1B receptors, since they were reversed by the 5-HT1B/1D antagonist GR 127935 (3 mg/kg), but not by the 5-HT1A antagonist WAY-100635 (1 mg/kg). None of the behavioural effects of RU-24969 are consistent with a selective action to enhance mesolimbic DA function. Rather, global activation of 5-HT1B receptors appear to exert a general disruptive effect on operant responding.
Repeated administration of the 5-HT(1)B/(1)A agonist, RU 24969, facilitates the acquisition of MDMA self-administration: role of 5-HT(1)A and 5-HT(1)B receptor mechanisms.[Pubmed:26856853]
Psychopharmacology (Berl). 2016 Apr;233(8):1339-47.
RATIONALE: 3,4 Methylenedioxymethamphetamine (MDMA) preferentially stimulates the release of serotonin (5-HT) that subsequently produces behavioral responses by activation of post-synaptic receptor mechanisms. The 5-HT1A and 5-HT1B receptors are both well localized to regulate dopamine (DA) release, and have been implicated in modulating the reinforcing effects of many drugs of abuse, but a role in acquisition of self-administration has not been determined. OBJECTIVES: This study was designed to determine the effect of pharmacological manipulation of 5-HT1A and 5-HT1B receptor mechanisms on the acquisition of MDMA self-administration. METHODS: The 5-HT1B/1A receptor agonist, RU 24969 (0.0 or 3.0 mg/kg, bid), was administered for 3 days in order to down-regulate both 5-HT1A and 5-HT1B receptors. Following the pretreatment phase, latency to acquisition of MDMA self-administration was measured. RESULTS: Repeated administration of RU 24969 significantly decreased the latency to acquisition and increased the proportion of animals that acquired MDMA self-administration. Dose-effect curves for the 5-HT1A-mediated hyperactivity produced by the 5-HT1A agonist, 8-OH-DPAT, and the 5-HT1B-mediated adipsic response produced by RU 24969 were shifted rightward, suggesting a desensitization of 5-HT1A and 5-HT1B receptor mechanisms. CONCLUSIONS: These data suggest that the initial reinforcing effects of MDMA are modulated by 5-HT1A and/or 5-HT1B receptor mechanisms. The potential impact of these changes on the DAergic response relevant to self-administration and a possible role in conditioned reinforcement pertaining to acquisition of self-administration are discussed.
