transmembrane

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

Endothelin-2 (49-69), human (Human endothelin-2), is a 21-amino-acid vasoactive peptide that binds to G-protein-coupled receptors ET-RA and ET-RB.

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.

Tezacaftor (VX-661) is a cystic fibrosis transmembrane conductance regulator (CFTR) corrector. Tezacaftor increases the number of functional CFTR proteins by promoting the proper folding and transport of mutant CFTR proteins to the cell surface, thereby restoring chloride channel function. Tezacaftor is commonly used in cystic fibrosis research.

V-9302 is a competitive antagonist of transmembrane glutamine flux. V-9302 selectively targets the amino acid transporter ASCT2 (SLC1A5) without affecting ASCT1. V-9302 inhibits ASCT2-mediated glutamine uptake in HEK-293 cells (IC50=9.6 μM). V-9302 can be used for research on tumor and amino acid transport

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

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

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).

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.

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

4BP-TQS is an allosteric agonist of α7 nAChRs.

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).

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.

Trivalent GalNAc-DBCO is a synthetic ligand composed of three GalNAc units linked to DBCO. Trivalent GalNAc-DBCO undergoes strain-promoted alkyne–azide cycloaddition (SPAAC) reactions with azide-containing molecules without the need for copper catalysis. Trivalent GalNAc-DBCO binds specifically to the asialoglycoprotein receptor (ASGPR), thereby directing conjugated molecules into hepatocytes for lysosomal degradation through receptor-mediated endocytosis. Trivalent GalNAc-DBCO is extensively applied in studies of liver-targeted drug delivery, targeted degradation strategies, and hepatocyte-specific molecular engineering.

TJU103 is a CD4 inhibitor that impedes the functionality of CD4 during activation, thereby suppressing autoreactive CD4+ T cells. In a mouse model of experimental autoimmune encephalomyelitis (EAE), TJU103 reduces monocyte infiltration in brain and spinal tissues. It downregulates Th1 and Th2 cytokine levels against proteolipid protein epitope 139-151 (PLPe) and exhibits inhibitory effects both after EAE symptom onset and subsequent antigen stimulation. TJU103 is applicable in research on autoimmune diseases such as EAE and multiple sclerosis (MS).

RWT9996 acts as a balanced GPR17 antagonist. It inhibits G protein activation and β-arrestin-2 recruitment induced by MDL-29951. Additionally, RWT9996 suppresses MDL-29951-induced ERK/CREB phosphorylation and inositol phosphate (IP1) accumulation. This compound is useful for researching neurological disorders.