Nav1.5
Nav1.5, encoded by SCN5A, is the main cardiac voltage-gated sodium channel and predominates the inward sodium current, INa, that drives the fast upstroke of the cardiac action potential[1]. Mechanistically, Nav1.5 supports myocardial excitability and electrical conduction, while its expression, localization, and biophysical properties are regulated through transcript structure, post-translational modification, and interacting proteins[2]. In disease models, SCN5A mutations and altered Nav1.5 function are linked to long QT syndrome, Brugada syndrome, conduction disease, cardiomyopathy, atrial fibrillation, and heart failure-associated arrhythmogenesis[1][2][3]. Compared with related sodium-channel isoforms, Nav1.5 is defined by its cardiac predominance, while the neonatal splice variant nNav1.5 shows distinct relevance in cancer-cell models[4]. In MDA-MB-231 breast cancer cells, nNav1.5 potentiates invasive behavior, and Nav1.5 regulates epithelial-to-mesenchymal transition and invasiveness through salt-inducible kinase-1[4][5]. For experimental applications, nNav1.5 blockers, propranolol, ranolazine combinations, and eslicarbazepine-related compounds have been used to inhibit Nav1.5 current or cancer-cell invasion in vitro[6][7][8].
References:
- [1]. Veerman CC, et al. The cardiac sodium channel gene SCN5A and its gene product NaV1.5: Role in physiology and pathophysiology. Gene. 2015 Dec 1;573(2):177-87. [Content Brief]
- [2]. Rook MB, et al. Biology of cardiac sodium channel Nav1.5 expression. Cardiovasc Res. 2012 Jan 1;93(1):12-23. [Content Brief]
- [3]. Bordachar P, et al. Contributions of a hemodynamic sensor embedded in an atrial lead in a porcine model. J Cardiovasc Electrophysiol. 2011 May;22(5):579-83. [Content Brief]
- [4]. Brackenbury WJ, et al. The neonatal splice variant of Nav1.5 potentiates in vitro invasive behaviour of MDA-MB-231 human breast cancer cells. Breast Cancer Res Treat. 2007 Jan;101(2):149-60. [Content Brief]
- [5]. Gradek F, et al. Sodium Channel Nav 1.5 Controls Epithelial-to-Mesenchymal Transition and Invasiveness in Breast Cancer Cells Through its Regulation by the Salt-Inducible Kinase-1. Sci Rep. 2019 Dec 9;9(1):18652. [Content Brief]
- [6]. Dutta S, et al. Discovery and evaluation of nNav 1.5 sodium channel blockers with potent cell invasion inhibitory activity in breast cancer cells. Bioorg Med Chem. 2018 May 15;26(9):2428-2436. [Content Brief]
- [7]. Lee A, et al. Propranolol inhibits neonatal Nav1.5 activity and invasiveness of MDA-MB-231 breast cancer cells: Effects of combination with ranolazine. J Cell Physiol. 2019 Dec;234(12):23066-23081. [Content Brief]
- [8]. Leslie TK, et al. Inhibitory Effect of Eslicarbazepine Acetate and S-Licarbazepine on Nav 1.5 Channels. Front Pharmacol. 2020 Oct 2;11:555047. [Content Brief]
All Product Categories
-
Nav1.5 Related Products (19)
Related Products (19)
- 1
-
Flecainide acetate
0 ImagesSynonyms: R-818Flecainide acetate (R-818) is a class 1C antiarrhythmic agent especially used for the management of supraventricular arrhythmia; works by blocking the Nav1.5 sodium channel in the heart, causing prolongation of the cardiac action potential.
-
ICA-121431
0 ImagesICA-121431 is a nanomolar potent and broad-spectrum voltage-gated sodium channel (Nav) blocker, shows equipotent selectivity for human Nav1.1 and Nav1.3 subtypes with IC50 values of 13 nM and 23 nM, respectively. ICA-121431 shows less potent inhibition of Nav1.2 (IC50=240 nM) and 1,000 fold selectivity against Nav1.4, Nav1.6, and the TTX-resistant human Nav1.5 and Nav1.8 channels (IC50s >10 μM).
-
PF-06456384 trihydrochloride
0 ImagesPF-06456384 trihydrochloride is an extremely potent and selective Nav1.7 sodium channel blocker (IC50: 0.01 nM for hNaV1.7; 75 nM for rNaV1.7; <0.1 nM for mNaV1.7). PF-06456384 trihydrochloride shows no significant analgesic efficacy in the mouse Formalin pain model.
-
TC-N 1752
0 ImagesTC-N 1752 is a potent and orally active inhibitor of Nav1.7, with IC50s of 0.17 μM, 0.3 μM, 0.4 μM, 1.1 μM and 2.2 μM at hNav1.7, hNav1.3, hNav1.4, hNaV1.5 and rNav1.8, respectively. TC-N 1752 also inhibits tetrodotoxin-sensitive sodium channels. TC-N 1752 shows analgesic efficacy in the Formalin model of pain.
-
GDC-0310
0 ImagesGDC-0310 is a selective acyl-sulfonamide Nav1.7 inhibitor, with an IC50 of 0.6 nM for hNav1.7.
-
ERG-IN-7
0 ImagesCat. No.: HY-184190ERG-IN-7 is a Nav1.5, Cav1.2 and Kv11.1 inhibitor with IC50 values of 10.34 μM, 21.01 μM, and 16.385 μM for human Nav1.5, Cav1.2, and Kv11.1, respectively. ERG-IN-7 prolongs action potentials, reduces conduction velocity, and restores cardiac function. ERG-IN-7 can be used for the research of ventricular arrhythmia.
-
MTSET chloride
0 ImagesCat. No.: HY-W699451MTSET chloride is a membrane-impermeable, thiol-specific reagent that primarily acts as an inhibitor of the Nav1.5 sodium channel. MTSET chloride reduces the peak sodium current amplitude of most mutant Nav1.5 channels, induces a hyperpolarizing shift in steady-state inactivation, and slows the recovery process, but shows no activity against wild-type and non-inactivating Nav1.5 channel mutants. MTSET chloride reacts covalently with T336C mutant P2X2 receptors, partially reversibly blocks ATP-induced cation currents, and exerts no effect on wild-type P2X2 receptors.
-
Nav1.5-IN-1
0 ImagesCat. No.: HY-181063CAS No.: 899207-91-1Nav1.5-IN-1 is a selective Nav1.5 inhibitor with an IC50 of 1.38 μM. Nav1.5-IN-1 shows selectivity over other Nav subtypes. Nav1.5-IN-1 reduces cardiac conduction in isolated rat hearts.Nav1.5-IN-1 can be used for the research of arrhythmias.
-
Funapide
0 ImagesSynonyms: TV 45070; XEN402Funapide (TV 45070; XEN402) is an orally active inhibitor of voltage-gated sodium channels (VGSC) in the peripheral nervous system with IC50 values ??of 84 nM and 54 nM for Nav1.5 and Nav1.7, respectively. Funapide has analgesic effects.
-
AA43279
0 ImagesAA43279 is an in gamma-aminobutyric acid (GABA) fast-firing interneurons located activator for Nav1.1 channel (SCN1A) with an EC50 of 9.5 μM. AA43279 enhances specific neuronal firing activity in vitro, and exhibits anticonvulsant activity in rat MEST model.
-
GpTx-1 TFA
0 ImagesCat. No.: HY-P1681APurity: 99.56%GpTx-1 TFA is a peptide-based NaV1.7 sodium channel antagonist isolated from the venom of the Chilean spider Grammostola porter. GpTx-1 TFA demonstrates potent inhibitory activity against the NaV1.7 channel with an IC50 value of 10 nM, while exhibiting excellent selectivity for NaV1.4 (IC50 = 0.301 μM) and NaV1.5 (IC50 = 4.20 μM), showing >20-fold and >950-fold selectivity respectively.
-
ProTx-I
0 ImagesCat. No.: HY-P1073CAS No.: 484598-35-8ProTx-I is a toxin derived from Thrixopelma pruriens and a peptide inhibitor targeting TTX-resistant sodium channels. ProTx-I interacts with voltage sensors of multiple domains such as NaV1.7, reduces neuronal excitability through allosteric modulation of channel gating and alteration of voltage dependence. The IC50 values of ProTx-I against human NaV1.7, NaV1.2, NaV1.6, and NaV1.5 are 95 nM, 104 nM, 21 nM, and 358 nM, respectively; ProTx-I also potently inhibits Ba2+ currents of hCav3.1, while its inhibitory potency against hCav3.2 is approximately 160-fold lower. ProTx-I is applicable to the research of chronic pain.
-
Sodium Channel inhibitor 1
0 ImagesSodium Channel inhibitor 1 is a state-dependent voltage-gated NaV1.7 inhibitor with an IC50 of 0.087 μM. Sodium Channel inhibitor 1 can be used for research of pain.
-
Phrixotoxin 3
0 ImagesCat. No.: HY-P1218CAS No.: 880886-00-0Phrixotoxin 3 is a potent blocker of voltage-gated sodium channels, with IC50s of 0.6, 42, 72, 288, 610 nM for NaV1.2, NaV1.3, NaV1.4, NaV1.1 and NaV1.5, respectively. Phrixotoxin 3 modulates voltage-gated sodium channels with properties similar to those of typical gating-modifier toxins, both by causing a depolarizing shift in gating kinetics and by blocking the inward component of the sodium current.
-
hERG-IN-3
0 ImagesCat. No.: HY-175289hERG-IN-3 is an orally active hERG blocker with an IC50 of 44.5 nM. hERG-IN-3 exhibits a Ki for β2-adrenergic receptor of 14 nM. hERG-IN-3 exhibits the skeletal muscle Nav1.4 and sodium channel-blocking activities (IC50 = 4.4 μM, 3-fold increasement than hNav1.5). hERG-IN-3 displays a potent antimyotonic activity in an animal model. hERG-IN-3 can be used for the study of Myotonia Congenita.
-
GpTx-1
0 ImagesCat. No.: HY-P1681CAS No.: 1661050-12-9GpTx-1 is a peptide-based NaV1.7 sodium channel antagonist isolated from the venom of the Chilean spider Grammostola porter. GpTx-1 demonstrates potent inhibitory activity against the NaV1.7 channel with an IC50 value of 10 nM, while exhibiting excellent selectivity for NaV1.4 (IC50 = 0.301 μM) and NaV1.5 (IC50 = 4.20 μM), showing >20-fold and >950-fold selectivity respectively.
-
Ceratotoxin-1
0 ImagesCat. No.: HY-P5811Synonyms: CcoTx1; β-TRTX-cm1aCeratotoxin-1 (CcoTx1), a peptide toxin, is an voltage-gated sodium channel subtypes inhibitor. Ceratotoxin-1 inhibits Nav1.1/β1, Nav1.2/β1, Nav1.4/β1, and Nav1.5/β1 with IC50 of 523 nM, 3 nM, 888 nM, and 323 nM, respectively. Ceratotoxin-1 also inhibits Nav1.8/β1.
-
GS-462808
0 ImagesCat. No.: HY-120774CAS No.: 1354198-41-6GS-462808 is an oral active late sodium current inhibitor (Late INai) of the cardiac Nav1.5 channel with the IC50 of 1.33 μM. GS-462808 can be used for study of arrhythmia.
-
DPP8/9-IN-2
0 ImagesCat. No.: HY-175226CAS No.: 3109603-86-0DPP8/9-IN-2 (Compound 21) is a DPP8/9 inhibitor with IC50 values of 0.22 nM and 3 nM, respectively, and Ki values of 2.9 nM and 6 nM, respectively . DPP8/9-IN-2 has certain cardiotoxicity, with IC50 values of 0.7 μM, 29.0 μM and 27.7 μM for hERG potassium channel, Nav1.5 sodium channel and Cav1.2 calcium channel, respectively. DPP8/9-IN-2 can be used in the research of diseases such as tumors.
- 1
