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Riluzole (RP-54274, PK 26124)

Alias: PK 26124, RP 54274, PK26124, RP54274, RP-54274, PK-26124;Rilutek
Cat No.:V1078 Purity: ≥98%
Riluzole (formerly PK26124, RP54274, RP-54274, PK-26124;Rilutek),an anticonvulsant of the Na+channelblocker class, is a glutamate release inhibitor with neuroprotective, anticonvulsant, anxiolytic and anesthetic activities.
Riluzole (RP-54274, PK 26124)
Riluzole (RP-54274, PK 26124) Chemical Structure CAS No.: 1744-22-5
Product category: GluR
This product is for research use only, not for human use. We do not sell to patients.
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100mg
250mg
500mg
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2g
5g
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Other Forms of Riluzole (RP-54274, PK 26124):

  • Riluzole HCl (RP-54274, PK 26124)
  • Riluzole-13C,15N2 (PK 26124-13C,15N2)
Official Supplier of:
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Top Publications Citing lnvivochem Products
Purity & Quality Control Documentation

Purity: ≥98%

Product Description

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.

Biological Activity I Assay Protocols (From Reference)
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].
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].
Animal Protocol
8 mg/kg i.p.
Rodent model of transient global cerebral ischemia
ADME/Pharmacokinetics
Absorption, Distribution and Excretion
Riluzole is well-absorbed (approximately 90%), with average absolute oral bioavailability of about 60% (CV=30%). A high fat meal decreases absorption, reducing AUC by about 20% and peak blood levels by about 45%.
Metabolism / Metabolites
Riluzole is extensively metabolized to six major and a number of minor metabolites, which have not all been identified to date. Metabolism is mostly hepatic, consisting of cytochrome P450–dependent hydroxylation and glucuronidation. CYP1A2 is the primary isozyme involved in N-hydroxylation; CYP2D6, CYP2C19, CYP3A4, and CYP2E1 are considered unlikely to contribute significantly to riluzole metabolism in humans.
Riluzole has known human metabolites that include 4-hydroxy-riluzole, 7-hydroxy-riluzole, 5-hydroxy-riluzole, and N-Hydroxyriluzole.
Riluzole is extensively metabolized to six major and a number of minor metabolites, which have not all been identified to date. Metabolism is mostly hepatic, consisting of cytochrome P450–dependent hydroxylation and glucuronidation. CYP1A2 is the primary isozyme involved in N-hydroxylation; CYP2D6, CYP2C19, CYP3A4, and CYP2E1 are considered unlikely to contribute significantly to riluzole metabolism in humans.
Half Life: The mean elimination half-life of riluzole is 12 hours (CV=35%) after repeated doses.
Biological Half-Life
The mean elimination half-life of riluzole is 12 hours (CV=35%) after repeated doses.
Toxicity/Toxicokinetics
Toxicity Summary
The mode of action of riluzole is unknown. Its pharmacological properties include the following, some of which may be related to its effect: 1) an inhibitory effect on glutamate release (activation of glutamate reuptake), 2) inactivation of voltage-dependent sodium channels, and 3) ability to interfere with intracellular events that follow transmitter binding at excitatory amino acid receptors.
Hepatotoxicity
Serum aminotransferase elevations occur in approximately up to 12% of patients on long term riluzole therapy, but elevations above 3 times the upper limit of normal (ULN) occur in less than 3% of patients. These elevations are usually mild-to-moderate in severity and are rarely associated with symptoms. Most elevations resolve spontaneously, but persistent or marked elevations require drug discontinuation or dose modification. Routine monitoring of serum aminotransferase levels is recommended for the first 6 months of therapy. Clinically apparent liver injury due to riluzole is rare, but several cases have been reported, arising after 1 to 12 months of therapy and characterized by a hepatocellular or mixed pattern of serum enzyme elevations. Immunoallergic and autoimmune features were uncommon. Most cases were mild to moderate in severity and recovery was rapid upon drug discontinuation, but evidently fatal cases have been reported to the sponsor.
Likelihood score: C (probable rare cause of clinically apparent liver injury).
Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Limited information indicates that maternal doses of riluzole up to 100 mg daily produce low levels in milk and would not be expected to cause any adverse effects in breastfed infants, especially if the infant is older than 2 months. Until more data are available, use riluzole with caution, particularly when breastfeeding a newborn.
◉ Effects in Breastfed Infants
Relevant published information was not found as of the revision date.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.
Protein Binding
96% bound to plasma proteins, mainly to albumin and lipoprotein over the clinical concentration range.
Toxicity Data
LD50: 85 mg/kg (p.o., mice) (L1859)
LD50: 34.5 mg/kg (i.v, mice) (L1859)
LD50: 45 mg/kg (p.o., rat) (L1859)
LD50: 21 mg/kg (i.v, mice) (L1859)
References

[1]. Neuroprotective agent riluzole potentiates postsynaptic GABA(A) receptor function. Neuropharmacology. 2002 Feb;42(2):199-209.

[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.

Additional Infomation
Pharmacodynamics
Riluzole, a member of the benzothiazole class, is indicated for the treatment of patients with amyotrophic lateral sclerosis (ALS). Riluzole extends survival and/or time to tracheostomy. It is also neuroprotective in various in vivo experimental models of neuronal injury involving excitotoxic mechanisms. The etiology and pathogenesis of amyotrophic lateral sclerosis (ALS) are not known, although a number of hypotheses have been advanced. One hypothesis is that motor neurons, made vulnerable through either genetic predisposition or environmental factors, are injured by glutamate. In some cases of familial ALS the enzyme superoxide dismutase has been found to be defective.
BF-37 interferes directly with cellular processes of the immune system of the skin, thereby diminishing the inflammation that underlies the reddening and itching.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C8H5F3N2OS
Molecular Weight
234.2
Exact Mass
234.007
CAS #
1744-22-5
Related CAS #
Riluzole hydrochloride;850608-87-6;Riluzole-13C,15N2;1215552-03-6
PubChem CID
5070
Appearance
White to yellow solid powder
Density
1.6±0.1 g/cm3
Boiling Point
296.3±50.0 °C at 760 mmHg
Melting Point
116-118ºC
Flash Point
133.0±30.1 °C
Vapour Pressure
0.0±0.6 mmHg at 25°C
Index of Refraction
1.615
LogP
2.84
Hydrogen Bond Donor Count
1
Hydrogen Bond Acceptor Count
7
Rotatable Bond Count
1
Heavy Atom Count
15
Complexity
238
Defined Atom Stereocenter Count
0
InChi Key
FTALBRSUTCGOEG-UHFFFAOYSA-N
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)
Chemical Name
6-(trifluoromethoxy)-1,3-benzothiazol-2-amine
Synonyms
PK 26124, RP 54274, PK26124, RP54274, RP-54274, PK-26124;Rilutek
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
DMSO: 47 mg/mL (200.7 mM)
Water:<1 mg/mL
Ethanol:47 mg/mL (200.7 mM)
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.

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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.
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 corn oil and mix evenly.


 (Please use freshly prepared in vivo formulations for optimal results.)
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.

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Note: Chemical formula is case sensitive: C12H18N3O4  c12h18n3o4
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In vivo Formulation Calculator (Clear solution)
Step 1: Enter information below (Recommended: An additional animal to make allowance for loss during the experiment)
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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.
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Clinical Trial Information
Riluzole in Patients With Spinocerebellar Ataxia Type 7
CTID: NCT03660917
Phase: Phase 2/Phase 3    Status: Recruiting
Date: 2024-12-02
Effect of Riluzole as a Symptomatic Approach in Patients With Chronic Cerebellar Ataxia
CTID: NCT00202397
Phase: Phase 2    Status: Completed
Date: 2024-12-02
Evaluate the Safety of Neuronata-R® Inj. Suspended With HypoTHermosol® FRS (HTS-FRS) in Patients With ALS
CTID: NCT06676423
Phase: Phase 1    Status: Completed
Date: 2024-11-06
Effectiveness Assessment of Riluzole in the Prevention of Oxaliplatin-induced Peripheral Neuropathy.
CTID: NCT03722680
Phase: Phase 2    Status: Suspended
Date: 2024-11-04
Evaluation the Efficacy and Safety of Mutiple Lenzumestrocel (Neuronata-R® Inj.) Treatment in Patients With ALS
CTID: NCT04745299
Phase: Phase 3    Status: Active, not recruiting
Date: 2024-10-03
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Riluzole and Sorafenib Tosylate in Treating Patients With Advanced Solid Tumors or Melanoma
CTID: NCT01303341
Phase: Phase 1    Status: Active, not recruiting
Date: 2024-09-19


Repurposing Riluzole for Cancer-Related Cognitive Impairment: a Pilot Trial
CTID: NCT06580002
Phase: Phase 2    Status: Not yet recruiting
Date: 2024-08-30
Riluzole in Combination With mFOLFOX6 and Bevacizumab in Treating Patients With Metastatic Colorectal Cancer
CTID: NCT04761614
Phase: Phase 1    Status: Active, not recruiting
Date: 2024-05-16
Treatment Combining Riluzole and IFB-088 in Bulbar Amyotrophic Lateral Sclerosis (TRIALS Protocol)
CTID: NCT05508074
Phase: Phase 2    Status: Active, not recruiting
Date: 2024-03-08
The Role of Glutamatergic Function in the Pathophysiology of Treatment-resistant Schizophrenia
CTID: NCT06270108
PhaseEarly Phase 1    Status: Recruiting
Date: 2024-03-05
Riluzole in Treating Patients With Stage III or Stage IV Melanoma That Cannot Be Removed by Surgery
CTID: NCT00866840
Phase: Phase 2    Status: Completed
Date: 2024-01-19
RiLuzole to Reduce Atrial FIb Study Using Holter Monitoring
CTID: NCT05292209
Phase: Phase 2    Status: Recruiting
Date: 2023-11-24
Masitinib in Combination With Riluzole for the Treatment of Patients Suffering From Amyotrophic Lateral Sclerosis (ALS)
CTID: NCT02588677
Phase: Phase 2/Phase 3    Status: Completed
Date: 2023-09-29
Trial of Safety, Tolerability and Efficacy of Trametinib (SNR1611) in Patients With Amyotrophic Lateral Sclerosis (ALS)
CTID: NCT04326283
Phase: Phase 1/Phase
PROTEIN MISFOLDING, AMYOTROPHIC LATERAL SCLEROSIS AND GUANABENZ: A PHASE II RCT WITH FUTILITY DESIGN
CTID: null
Phase: Phase 2    Status: Ongoing
Date: 2016-02-29
A randomized, double-blind, controlled, monocenter, pivotal phase IIb study to evaluate the efficacy and safety of riluzole versus mexiletine in patients with non dystrophic myotonia mutated in SCN4A or CLCN1 genes.
CTID: null
Phase: Phase 2    Status: Ongoing
Date: 2015-11-03
A randomized, double blind, double-dummy placebo controlled, 3-way cross-over study to determine the test-retest reliability of, and the effect of oral retigabine and riluzole on, peripheral motor nerve excitability measurements in patients with ALS.
CTID: null
Phase: Phase 2    Status: Completed
Date: 2015-08-17
MS-SMART: A Multi-Arm Phase IIb Randomised, Double Blind Placebo-Controlled Clinical Trial Comparing The Efficacy of Three Neuroprotective Drugs in Secondary Progressive Multiple Sclerosis
CTID: null
Phase: Phase 2    Status: Completed
Date: 2014-04-01
A Phase IIb, multi-national, double-blind, randomised, placebo-controlled study to evaluate the safety, tolerability and efficacy of CK-2017357 in patients with amyotrophic lateral sclerosis (ALS)
CTID: null
Phase: Phase 2    Status: Completed
Date: 2013-02-08
Offene Verträglichkeitsstudie zur Evaluierung einer subkutanen Injektionslösung von 100 mg Anakinra in Kombination mit Riluzol bei Patienten mit Amyotropher Lateralsklerose (ALS).
CTID: null
Phase: Phase 2    Status: Completed
Date: 2010-12-06
Evaluation of efficacy of lithium salts therapy in patients with Amyotrophic Lateral Sclerosis.
CTID: null
Phase: Phase 2    Status: Completed
Date: 2009-02-24
A Phase II Proof-of-Concept, Randomized, Double-blind, Vehicle-controlled Study, Including an Open-label Comparison to an Active Control, To Assess the Efficacy and Safety/Tolerability of Topical Riluzole in Patients with Stable Plaque-type Psoriasis
CTID: null
Phase: Phase 2    Status: Completed
Date: 2008-02-14
Phase IIa, single-center, randomized, double-blind, vehicle-controlled study to determine the efficacy and safety/tolerability of a topical riluzole formulation in patients with atopic eczema
CTID: null
Phase: Phase 2    Status: Completed
Date: 2007-04-20
Evaluation of the pharmacokinetic profile of Riluzole (XRP4274) and RPR112512 following multiple oral administrations of XRP4274 for 8 days
CTID: null
Phase: Phase 4    Status: Completed
Date: 2004-11-24

Biological Data
  • 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
  • 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
  • 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
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