MTSET chloride 

MTSET 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^[1][2][3].

MTSET chloride (1 mM; 5 min) significantly inhibits Na⁺ currents in tsA201 cells expressing Nav1.5 D4S6 cysteine mutants F1760C, V1763C, Y1767C, S1759C, V1764C and M1766C, with the strongest inhibitory effect on Y1767C (a 42.1% decrease)^[1].
MTSET chloride (1 mM; 15 min) inhibits ATP-evoked currents in Xenopus oocytes expressing concatenated tetrameric rat P2X2 receptors in a position-dependent manner: the inhibitory effect is stronger when the mutated subunit is located near the amino terminus, and weaker when located near the carboxyl terminus; the maximum inhibition rate of single-mutant constructs reaches up to 50.2%, while the minimum inhibition rate of single-wild-type constructs is only 24.2%^[2].
MTSET chloride (1 mM; 15 min) inhibits ATP-evoked currents in Xenopus oocytes expressing tandem hexameric rat P2X2 receptors in a position-dependent manner; the inhibition is significant (34.2%) only when the mutant subunit is located at the amino terminus, whereas the inhibition is attenuated (58.1%) only when the wild-type subunit is located at the amino terminus^[2].
MTSET chloride (100 μM; 10-40 sec) exerts a state-dependent modification effect on the I248C mutant Ci-HV channel expressed in Xenopus oocytes, modifying the channel only when it is in the open (depolarized) state, with a second-order rate constant of 5620 M^-1s^-1[3].
MTSET chloride exhibits state-dependent accessibility to the V252C mutant Ci-HV channel expressed in Xenopus oocytes, and only modifies the channel when it is in the open (depolarized) state^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

233.78

C₆H₁₆ClNO₂S₂

CS(SCC[N+](C)(C)C)(=O)=O.[Cl-]

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. O’Leary M E, et al. MTSET modification of D4S6 cysteines stabilize the fast inactivated state of Nav1. 5 sodium channels[J]. Frontiers in Pharmacology, 2015, 6: 118.

  [2]. Stoop R, et al. Contribution of individual subunits to the multimeric P2X(2) receptor: estimates based on methanethiosulfonate block at T336C. Mol Pharmacol. 1999 Nov;56(5):973-81.

  [3]. Gonzalez C, et al. Strong cooperativity between subunits in voltage-gated proton channels. Nat Struct Mol Biol. 2010 Jan;17(1):51-6.