CAS 1262618-39-2 GS967 Powder Potent Late INa Blocker for Cardiac Electrophysiology Research

Premium GS967 GS-458967 crystalline powder CAS 1262618-39-2, highly selective cardiac late sodium current inhibitor lab-grade reagent. In stock for cardiac electrophysiology and anti-arrhythmia research.
GS967 (CAS 1262618-39-2) Late Sodium Current Inhibitor | Selective Persistent I_Na Blocker for Anti-Arrhythmic & Anti-Epileptic Research

GS967 CAS 1262618-39-2
Selective Late Sodium Current (Persistent I_Na) Inhibitor

GS967 (CAS 1262618-39-2), also GS-458967, is a potent and selective inhibitor of the late (persistent) sodium current (late I_Na) with IC50 values of 0.13 and 0.21 uM in ventricular myocytes and isolated hearts. It shows ~42-fold preference for persistent over peak current and exerts anti-arrhythmic and anti-epileptic effects without broadly blocking other cardiac ion channels. Molecular formula C14H7F6N3O, MW 347.22. Research-grade with COA.

Late Sodium Current Persistent I_Na Nav1.5 Antiarrhythmic Antiepileptic GS-458967 Cardiac Ion Channel
347.22
MW (C14H7F6N3O)
0.13 uM
Late I_Na IC50
~42x
persistent vs peak

Molecular Information

Name: GS967
CAS: 1262618-39-2
Formula: C14H7F6N3O
MW: 347.22 g/mol
Class: Triazolopyridine
Core: 6-[4-(trifluoromethoxy)phenyl]-3-(trifluoromethyl)-[1,2,4]triazolo[4,3-a]pyridine
Target: Late/persistent I_Na (Nav1.5)
IC50: 0.13 uM (myocytes)
Selectivity: ~42x persistent vs peak
Appearance: White solid powder
Synonyms: GS-458967
Storage: -20 C
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CAS Number
1262618-39-2
⚖️
Molecular Weight
347.22
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Primary Activity
Late I_Na Inhibitor
Purity
≥98%

Product Technical Specifications

Complete physicochemical properties and QC parameters for GS967 (CAS 1262618-39-2)

📋 Physicochemical Properties

  • Product NameGS967 (GS-458967)
  • IUPAC Core6-[4-(trifluoromethoxy)phenyl]-3-(trifluoromethyl)-[1,2,4]triazolo[4,3-a]pyridine
  • CAS Number1262618-39-2
  • SynonymsGS-458967; GS 458967; GS-967
  • Molecular FormulaC14H7F6N3O
  • Molecular Weight347.22 g/mol
  • SourceSynthetic small molecule
  • AppearanceWhite solid powder
  • Melting PointNot reported
  • Water SolubilityInsoluble
  • Organic SolubilityDMSO ~45 mg/mL; ethanol ~46 mg/mL
  • Compound ClassTriazolopyridine / late-Na blocker
  • HS Code2934.99

🔬 Quality Control & Handling

  • Purity (HPLC)≥98%
  • FormSolid powder
  • Primary TargetLate / persistent sodium current (I_Na,L)
  • Pathway ReadoutReduced late I_Na; shortened action-potential duration
  • Selectivity~42x persistent vs peak I_Na; spares Ca2+/K+ channels
  • Storage Condition-20 C, sealed, protect from light
  • Solution StabilityAliquot DMSO stocks; avoid freeze-thaw
  • ShippingRoom-temp stable (per testing) / blue ice optional
  • QC DocumentationCOA / HPLC / NMR / MS / MSDS
  • Pack Sizes1g / 5g / 10g / 100g / 1KG
  • Stock StatusIn Stock
  • Use StatementResearch use only; not for human/clinical use

Key Molecular Targets & Pathway Nodes

GS967's therapeutic interest centers on the late (persistent) component of the cardiac and neuronal sodium current, which becomes pathological in disease.

🧬 Nav1.5 (cardiac Na+ channel) 🌊 Late / Persistent I_Na ⚡ Peak I_Na (weak, ~42x less) 🫀 Cardiac Myocytes 🧠 Neurons / CNS 🔥 Arrhythmia Triggers (EAD/DAD) 🧠 Seizure Threshold 📉 Action Potential Duration 🧬 Ca2+ Handling 🔬 Ion-Channel Selectivity 🩸 Ischemia Models 🧫 Epilepsy Models

How GS967 Works: Silencing the Pathological Late Sodium Leak

By preferentially blocking persistent sodium current, GS967 curbs the late inward Na+ load that destabilizes hearts and neurons

1

Persistent vs Peak Sodium Current

Voltage-gated sodium channels (notably Nav1.5 in heart) open transiently (peak current) but a small fraction fail to fully inactivate, producing a tiny 'late' (persistent) inward Na+ current (I_Na,L). In disease (ischemia, hypoxia, mutations) this late current is amplified, prolonging the action potential and promoting arrhythmias and excitability disorders.

2

Selective Late-Current Blockade

GS967 binds to inhibit the late/persistent I_Na with IC50 ~0.13 uM in myocytes and ~0.21 uM in isolated hearts, showing ~42-fold preference for persistent over peak current. This spares normal rapid depolarization while removing the pathological leak.

3

Electrical Stabilization & Anti-Seizure Effect

Reducing late I_Na lowers intracellular Na+ (and secondary Ca2+ via NCX), shortens pathologically prolonged action potentials, and reduces early- (EAD) and delayed- (DAD) afterdepolarizations that seed arrhythmias. In neurons the same mechanism raises seizure threshold, underpinning anti-epileptic activity — without broad sedation.

⚖️ GS967 vs Ranolazine vs Flecainide

  • GS967 (this)Selective persistent I_Na; ~42x vs peak; anti-arrhythmic & anti-epileptic
  • RanolazineLate I_Na inhibitor; anti-anginal (same mechanism)
  • FlecainideBroad use-dependent Na+ blocker; pro-arrhythmic risk
  • Selectivity EdgeGS967 spares peak & most other channels
  • Research UseLate-current pathology models
  • DistinctionPreferential persistent-current targeting

♻️ Downstream Biological Consequences

  • Na+ LoadReduced late inward Na+
  • Ca2+ HandlingLower Na+/Ca2+ exchanger load
  • APDShortened pathologically prolonged AP
  • ArrhythmiaFewer EAD/DAD triggers
  • NeuronElevated seizure threshold
  • SafetyMinimal effect on peak/L-type/Ca-K channels

Research Applications & Models

Late sodium current is a validated but under-exploited drug target in cardiology and neurology.

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Anti-Arrhythmic Research

Studied for suppressing EAD- and DAD-mediated extrasystoles in atrial and ventricular preparations, including ischemia and catecholamine models — a clean late-I_Na mechanism.

EAD / DAD
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Anti-Epileptic Models

Demonstrates anticonvulsant activity and protection against premature lethality in Scn2a epilepsy models, raising seizure threshold without sedation.

Seizure Threshold
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Cardiac Ischemia / Reperfusion

Reduces ischemia-induced repolarization alternans and ECG heterogeneity in porcine/canine models, protecting against arrhythmogenesis.

Ischemia
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Ion-Channel Selectivity

A precision tool to isolate persistent-Na vs peak-Na pharmacology; benchmarked against ranolazine and flecainide in cardiac myocyte assays.

Ion Channels
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SCN Mutant Models

Used in Nav1.5/SCN5A and SCN2A mutant contexts to probe gain-of-function sodium-channel pathologies.

SCN Mutants
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Action-Potential Research

Quantifies APD shortening and late-current contribution in guinea-pig and rabbit myocytes — establishing basal late I_Na as an APD determinant.

APD
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Long-QT / Repolarization

Explored where late Na+ blockade corrects acquired long-QT and drug-induced repolarization prolongation.

Long-QT
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Anti-Anginal Context

Shares the late-I_Na mechanism of ranolazine, supporting studies of myocardial oxygen-demand reduction in ischemic heart disease.

Anti-Anginal

Key Literature & Landmark Publications

Key references on late sodium current and GS967 pharmacology.

Bonatti R, et al. Selective late sodium current blockade with GS-458967 markedly reduces ischemia-induced atrial and ventricular repolarization alternans and ECG heterogeneity. Heart Rhythm. 2014;11(10):1827-35.
doi: 10.1016/j.hrthm.2014.06.017
Anderson LL, et al. Antiepileptic activity of preferential inhibitors of persistent sodium current. Epilepsia. 2014;55(8):1274-83.
doi: 10.1111/epi.12657
Song Y, Belardinelli L. Basal late sodium current is a significant contributor to the duration of action potential of guinea pig ventricular myocytes. Physiol Rep. 2017;5(10):e13295.
Landmark reference
Investigator report. GS967 (GS-458967) cardiac ion-channel profiling.
Landmark reference
Review. Persistent sodium current as a therapeutic target in arrhythmia and epilepsy.
Landmark reference

Available Sizes & Ordering

Research-grade GS967 (CAS 1262618-39-2) with full QC documentation; standard packs and bulk custom quantities supported.

TierPack SizeStock StatusSuitable ForLead Time
Standard1gIn StockLate-I_Na / cardiac ion-channel assaysSame/next-day ship
Medium5gIn StockIschemia & arrhythmia modelsSame/next-day ship
Large10gIn StockEpilepsy & neuronal excitability studiesSame/next-day ship
Bulk100gIn StockElectrophysiology & formulationQuote to confirm
Industrial1KGMade to orderPilot/production scale, CMO supplyBatch delivery

💡 Reference sizes shown above; for exact pricing and availability please contact us for a quote. Bulk orders qualify for tiered discounts.

Frequently Asked Questions (FAQ)

What is GS967?
GS967 (CAS 1262618-39-2), also GS-458967, is a potent, selective inhibitor of the late (persistent) sodium current (late I_Na) with IC50 ~0.13 uM in ventricular myocytes and ~0.21 uM in isolated hearts. It shows ~42-fold preference for persistent over peak sodium current. Formula C14H7F6N3O, MW 347.22.
What is 'late' sodium current and why target it?
After the big transient ('peak') sodium current that fires an action potential, a small fraction of channels fail to fully inactivate, producing a tiny lingering 'late' inward Na+ current. In ischemia, hypoxia or ion-channel mutations this late current is amplified, prolonging the action potential and fueling arrhythmias and seizures. Blocking it stabilizes electrical activity without crippling normal firing.
How does GS967 differ from ranolazine or flecainide?
All three touch sodium channels, but GS967 is the most selective for the persistent component (~42x over peak) and largely spares other cardiac ion channels, giving a clean late-I_Na mechanism. Ranolazine shares this late-I_Na mechanism (anti-anginal). Flecainide is a broad use-dependent blocker with pro-arrhythmic potential. GS967 also shows anti-epileptic activity absent from the others' primary use.
What readouts confirm activity?
Electrophysiology: reduced late I_Na (patch clamp) and shortened pathologically prolonged action-potential duration. In tissues, reduced EAD/DAD afterdepolarizations and repolarization alternans. It should not substantially suppress peak Na+, L-type Ca2+ or major K+ currents at therapeutic concentrations.
In which models is it studied?
Cardiac ischemia/reperfusion and arrhythmia (atrial/ventricular) models, long-QT and repolarization studies, and epilepsy models (including Scn2a mutant mice) where it raises seizure threshold without sedation.
How soluble is GS967 and how should it be prepared?
Soluble in DMSO (~45 mg/mL) and ethanol (~46 mg/mL), insoluble in water. For cell/electrophysiology dilute DMSO stock into bath solution (final DMSO minimal); active concentrations are low nanomolar to low micromolar. Store solid at -20 C; aliquot stocks.
Is QC documentation provided?
Every batch ships with a Certificate of Analysis (COA) including HPLC purity, NMR structural confirmation and MS data. MSDS/SDS, residual-solvent data and Certificates of Origin are available on request. Sample evaluation is available for qualified institutions — please contact us.

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Weight 0.25 g