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100mg |
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250mg |
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500mg |
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1g |
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2g |
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5g |
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10g |
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Purity: ≥98%
Riluzole (formerly PK26124, RP54274, RP-54274, PK-26124; Rilutek), an anticonvulsant of the Na+ channel blocker class, is a glutamate release inhibitor with neuroprotective, anticonvulsant, anxiolytic and anesthetic activities. Riluzole has been approved as a medication to treat amyotrophic lateral sclerosis. Riluzole acts by complex mechanism involving inhibition of voltage-dependent Na channels, high-voltage activated Ca and K channels, and inhibition of protein kinase C. It was suggested that this mechanism was involved in antioxidative processes.
ln Vitro |
Riluzole is an anticonvulsant that is a member of the use-dependent Na+ channel blocker family. It has an IC50 of 43 μM and inhibits GABA uptake as well. Riluzole consistently prolongs IPSCs at 20 μM, but it only slightly inhibits peak self-exposure to IPSCs. Furthermore, a significant, concentration-dependent, and easily reversible enhancement of the response to 2 μM GABA was observed with riluzole. After a prolonged co-exposure to 2 μM GABA and Riluzole at higher concentrations, particularly 300 μM, GABA currents demonstrated a notable desensitization. Riluzole has an EC50 of about 60 μM for increasing GABA response[1].
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ln Vivo |
In comparison to the vehicle tested in the same rats, systemic injection of Riluzole (8 mg/kg, i.p.; n = 6 rats) decreased the duration of ultrasound caused by painful stimulation of the knee joint. but did not lessen vocalizations that could be heard (P < 0.05). When compared to predose and vehicle, systemic administration of Riluzole (8 mg/kg, ip; n=19 rats) dramatically decreased vocalizations in arthritic rats (P<0.05 to 0.001). When compared to predose values, the length of audible and ultrasonic vocalizations elicited by painful stimulation of the knee was considerably reduced by administering Riluzole into the CeA (n = 8 rats; P < 0.05 to 0.01) [2].
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Animal Protocol |
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References |
[1]. He Y, et al. Neuroprotective agent riluzole potentiates postsynaptic GABA(A) receptor function. Neuropharmacology. 2002 Feb;42(2):199-209.
[2]. Thompson JM, et al. Small-conductance calcium-activated potassium (SK) channels in the amygdala mediate pain-inhibiting effects of clinically available riluzole in a rat model of arthritis pain. Mol Pain. 2015 Aug 28;11:51 |
Molecular Formula |
C8H5F3N2OS
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Molecular Weight |
234.2
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CAS # |
1744-22-5
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Related CAS # |
Riluzole hydrochloride;850608-87-6;Riluzole-13C,15N2;1215552-03-6
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Appearance |
Typically exists as solids (or liquids in special cases) at room temperature
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SMILES |
S1C(N([H])[H])=NC2C([H])=C([H])C(=C([H])C1=2)OC(F)(F)F
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InChi Key |
FTALBRSUTCGOEG-UHFFFAOYSA-N
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InChi Code |
InChI=1S/C8H5F3N2OS/c9-8(10,11)14-4-1-2-5-6(3-4)15-7(12)13-5/h1-3H,(H2,12,13)
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Chemical Name |
6-(trifluoromethoxy)-1,3-benzothiazol-2-amine
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Synonyms |
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HS Tariff Code |
2934.99.9001
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Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
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Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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Solubility (In Vitro) |
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Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (10.67 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (10.67 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (10.67 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
1 mM | 4.2699 mL | 21.3493 mL | 42.6985 mL | |
5 mM | 0.8540 mL | 4.2699 mL | 8.5397 mL | |
10 mM | 0.4270 mL | 2.1349 mL | 4.2699 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration: mg/mL;
Method for preparing DMSO stock solution: mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation::Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
NCT Number | Recruitment | interventions | Conditions | Sponsor/Collaborators | Start Date | Phases |
NCT05292209 | Recruiting | Drug: Riluzole 50 MG | Atrial Fibrillation Paroxysmal | University of Utah | June 15, 2022 | Phase 2 |
NCT04630444 | Completed | Drug: Riluzole | Posttraumatic Stress Disorder | Mclean Hospital | Early Phase 1 | March 16, 2017 |
NCT02796755 | Completed Has Results | Drug: Riluzole Drug: Placebo |
Inflammation Fatigue |
Emory University | April 2016 | Phase 4 |
NCT04819438 | Completed | Drug: Riluzole 50 mg Oral Film Drug: Rilutek 50Mg Tablet |
Bioequivalence | Cross Research S.A. | January 15, 2021 | Phase 1 |
NCT03679975 | Terminated Has Results | Drug: Riluzole Oral Soluble film (ROSF) 50 mg | Amyotrophic Lateral Sclerosis | Aquestive Therapeutics | April 4, 2018 | Phase 2 |
Inhibitory effects of systemically applied riluzole on vocalizations. a, b Riluzole (8 mg/kg, i.p.) had no effect on audible vocalizations (a) but inhibited ultrasonic vocalizations (b) to noxious stimulation of the knee joint compared to vehicle in normal naïve rats (n = 6). n.s. non-significant; *P < 0.05; paired t test. c, d Induction of arthritis resulted in a significant increase of audible (c) and ultrasonic (d) vocalizations evoked by noxious stimuli. Riluzole (8 mg/kg, i.p.; n = 19 rats) inhibited vocalizations of arthritic rats compared to predrug and vehicle (HBC, 30 %, i.p.; n = 16 rats). n.s. non-significant; *,**,***P < 0.05, 0.01, 0.001; repeated measures one-way ANOVA (compared to predrug) and unpaired t test (compared to vehicle) with Bonferroni posttests/correction. Bar histograms show mean ± SEM.[2]Small-conductance calcium-activated potassium (SK) channels in the amygdala mediate pain-inhibiting effects of clinically available riluzole in a rat model of arthritis pain. Mol Pain. 2015 Aug 28;11:51 td> |
Lack of effect of systemically applied riluzole on spinal withdrawal thresholds. Induction of arthritis significantly reduced hindlimb withdrawal thresholds measured by mechanical compression of the knee joint. Systemic application of vehicle (HBC, 30 %, i.p.; n = 11 rats) or riluzole (8 mg/kg, i.p.; n = 7 rats) had no effect compared to predrug values. Bar histograms show mean ± SEM. n.s. non-significant; ***P < 0.001; repeated measures one-way ANOVA with Bonferroni posttests.[2]Small-conductance calcium-activated potassium (SK) channels in the amygdala mediate pain-inhibiting effects of clinically available riluzole in a rat model of arthritis pain. Mol Pain. 2015 Aug 28;11:51 td> |
Involvement of SK, but not BK, channels in the CeA, but not BLA, in the inhibitory effects of riluzole in arthritis. a, b Systemic riluzole (8 mg/kg, i.p.) had no effect on audible (a) and ultrasonic (b) vocalizations compared to predrug values, when an SK channel blocker (apamin, 1 μM, concentration in the microdialysis probe, 15 min) was administered stereotaxically into the CeA of arthritic rats (n = 9 rats; 5 h postinduction). When ACSF was administered into the CeA, systemic riluzole inhibited vocalizations of arthritic rats significantly compared to predrug values (n = 9 rats). n.s. non-significant; **P < 0.01; paired t test. c, d Stereotaxic application of a BK channel blocker (charybdotoxin, ChTx, 1 μM, concentration in the microdialysis probe, 15 min) into the CeA (n = 5 rats) or stereotaxic application of apamin (1 μM, concentration in the microdialysis probe, 15 min) into the BLA (n = 6 rats) did not block the significant inhibitory effects of systemic riluzole on audible (c) and ultrasonic (d) vocalizations of arthritic rats compared to predrug values. n.s. non-significant; *,**P < 0.05; paired t test. Bar histograms show mean ± SEM.[2]Small-conductance calcium-activated potassium (SK) channels in the amygdala mediate pain-inhibiting effects of clinically available riluzole in a rat model of arthritis pain. Mol Pain. 2015 Aug 28;11:51 td> |