conductance

Glibenclamide (Glyburide) is an antidiabetic sulfonylurea derivative with actions similar to those of chlorpropamide.

Elexacaftor (VX-445) is a cystic fibrosis transmembrane conductance regulator (CFTR) corrector. It promotes the processing and trafficking of CFTR, increases the amount of CFTR on the cell surface, and improves the processing and trafficking of Phe508del CFTR protein.

BPO-27 racemate (BPO-27 (racemate)) is an effective CFTR inhibitor with IC50 of 8 nM.

Ataluren (PTC124) is a novel, orally administered drug that targets nonsense mutations. Ataluren is approved for use by the European Medicines Agency to treat Duchenne Muscular Dystrophy in patients aged 5 years and older who are able to walk.

Ivacaftor (VX-770) (VX-770) is a potentiator of CFTR targeting G551D-CFTR (EC50: 100 nM) and F508del-CFTR (EC50: 25 nM) in Fisher rat thyroid cells, respectively.

Lumacaftor (VRT 826809) is a CFTR modulator that corrects the folding and trafficking of CFTR protein. It enhances F508del-CFTR protein maturation in FRT cells (EC50: 100 nM).

GLPG1837 (ABBV-974) is an effective CFTR potentiator, with EC50s of 3 nM and 339 nM for F508del and G551D CFTR, respectively.

Nesolicaftor (PTI-428) specifically enhances cystic fibrosis transmembrane conductance regulator protein synthesis.

PPQ-102 (CFTR Inhibitor), an effective CFTR inhibitor, can completely inhibit CFTR chloride current (IC50: 90 nM).

Tezacaftor (VX661) is a small molecule that can be used as a corrector of the cystic fibrosis transmembrane conductance regulator (CFTR) gene function.

CFTR(inh)-172 (CFTR Inhibitor-172) is a voltage-independent, selective CFTR inhibitor.

GlyH-101 is a cell-permeable glycinyl hydrazone compound that blocks CFTR with Ki of 1.4 uM.

IOWH-032 (IOWH032) , a synthetic CFTR inhibitor, has been investigated for the treatment of cholera, diarrhea, and secretory diarrhea.

KM11060 is a novel corrector of the F508del-CFTR trafficking defect, Correcting F508del-CFTR trafficking, increasing the amount of functional CFTR at the plasma membrane.

CFTR corrector 2 (FDL169) is a novel and potent CFTR (Cystic fibrosis transmembrane conductance regulator) corrector for treating cystic fibrosis (CF) patients who carry the F508del mutation.

Icenticaftor (QBW251) is an orally active potentiator of the CFTR channel.

Rimtuzalcap (CAD-1883) (CAD-1883), a pioneering selective positive allosteric modulator of small-conductance calcium-activated potassium channels (SK channels), is employed in the study of movement disorders such as spinocerebellar ataxia (SCA) and essential tremor (ET).

(S)-(+)-Ibuprofen (Dexibuprofen) , is a non-steroidal anti-inflammatory drug (NSAID), inhibiting cyclooxygenase (COX).

GLPG2451 is an effective CFTR (Cystic Fibrosis Transmembrane Conductance Regulator) enhancer that potentiates cold-rescued F508del CFTR (EC50=11.1 nM), suitable for cystic fibrosis research.

CFTR corrector 4 is a potent and orally available transmembrane conductance regulator (CFTR) for cystic fibrosis and is a potent (R,R) type active enantiomer. CFTR corrector 4 increases CFTR levels on the cell surface and is a potential compound for the study of cystic fibrosis.

Cavosonstat (N91115) is an orally active S-nitrosoglutathione reductase (GSNOR) inhibitor that promotes cystic fibrosis transmembrane conductance regulator (CFTR) maturation and plasma membrane stabilization. As a CFTR stabilizer, Cavosonstat can be used to study cystic fibrosis.

Bamocaftor is a CFTR channel (DeltaF508-CFTR mutation) corrector for CF transmembrane conductance regulators designed to restore F508del-CFTR protein function. Combined use of tezacaftor and VX-561 for the treatment of cystic fibrosis patients with F508del/MF.

CFTR corrector 8 is a highly effective modulator of the cystic fibrosis transmembrane conductance regulator (CFTR). This compound is specifically designed for utilization in research related to cystic fibrosis, a genetic disorder primarily affecting the lungs and digestive system [1].

Benzthiazide (Lemazide) is used in the therapy of edema and hypertension. Like other thiazides, benzthiazide accelerates water loss from the body (diuretics). They inhibit Na+/Cl- reabsorption from the distal convoluted tubules in the kidneys. Thiazides also cause loss of potassium and an increase in serum uric acid. Thiazides are often used to treat hypertension, but their hypotensive effects are not necessarily due to their diuretic activity. Thiazides have been shown to prevent hypertension-related morbidity and mortality although the mechanism is not fully understood. Thiazides cause vasodilation by activating calcium-activated potassium channels (large conductance) in vascular smooth muscles and inhibiting various carbonic anhydrases in vascular tissue.