Chloride Channel Modulators

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219671 CFTR Inhibitor II, GlyH-101 - CAS 328541-79-3 - Calbiochem CFTR Inhibitor II, GlyH-101, CAS 328541-79-3, is a cell-permeable potent, selective and reversible open-channel blocker of CFTR (Ki = 4.3 µM in CFTR-expressing FRT cells).  
219672 CFTR Inhibitor III, OXO-172 - Calbiochem The CFTR Inhibitor III, OXO-172 controls the biological activity of CFTR. This small molecule/inhibitor is primarily used for Biochemicals applications.  
309795 DIDS, Disodium Salt - CAS 53005-05-3 - Calbiochem Binds covalently and irreversibly to the outer surface of human erythrocyte membranes.  
484100 5-Nitro-2-(3-phenylpropylamino)benzoic Acid - CAS 107254-86-4 - Calbiochem Potent Cl⁻ channel blocker (IC₅₀ = 100 nM-100 µM), depending on channel subtype and assay method.  
528105 Picrotoxin, Anamirta cocculin - CAS 124-87-8 - Calbiochem A potent antagonist of GABA receptors (IC₅₀ = 240 nM) at synapses in the central nervous system.  
SML1813 Ani9 2-(4-chloro-2-methylphenoxy)-N-[(2-methoxyphenyl)methylideneamino]-acetamide (Ani9), the most potent inhibitor, is the structural analog of Ani7. It may be considered as a novel candidate for drug therapy of cancer, hypertension, pain, diarrhea and asthma.
Ani9 is a potent and highly selective anoctamin1 (ANO1)/transmembrane protein 16A (TMEM16A) inhibitor that completely inhibited ANO1 chloride current with submicromolar potency. Ani9 does not affect the intracellular calcium signaling and CFTR chloride channel activity.
B104 tert-Butyl bicyclo[2.2.2]phosphorothionate solid GABAA receptor antagonist; chloride channel blocker; extremely potent convulsant.
C6617 CBIQ ≥98% (HPLC), solid CBIQ is an activator of the cystic fibrosis transmembrane conductance regulator (CFTR) and the intermediate-conductance calcium-sensitive K+ channel (KCNN4). CBIQ is a novel tool for a new ion channel; first activator of ΔF508 CFTR, the mutant form of CFTR chloride channel present in 75% of cystic fibrosis patients. Other benzoquinolines act at the normal CFTR but not at ΔF508 CFTR. CBIQ also activates KCNN4, which hyperpolarizes airway epithelial cells to promote anion flux, a further benefit in cystic fibrosis.
C2992 CFTR(inh)-172 ≥98% (HPLC), powder CFTR(inh)-172 is an inhibitor of the cystic fibrosis transmembrane conductance regulator (CFTR). With a Ki = 300 nM,. CFTR(inh)-172 leads to rapid, reversible and voltage-independent inhibition; it is an antidiarrheal agent in animals. CTFR(inh)-172 may be a useful tool to study animal models of cystic fibrosis and intestinal fluid loss in cholera and other secretory diarrheas. CTFR(inh)-172 is structurally-unrelated to known, but non-specific CFTR inhibitors DPC, NPPB (Cat. No. N4779) and Glibenclamide.
C5238 Chlorotoxin from Leiurus quinquestriatus (north Africa) recombinant, expressed in E. coli, ≥98% (HPLC), lyophilized powder Potent blocker of small-conductance Cl- channels.
D9190 DCEBIO ≥98% (HPLC), solid DCEBIO facilitates Cl secretion in the epithelia by activating K+ and Cl currents.
D129 R-(+)-DIOA ≥98% (HPLC), solid Potent [K+,Cl-]-cotransport inhibitor that shows no side effects on the bumetanimide-sensitive [Na+,K+,Cl-]-cotransport system.
SML1157 Eact ≥98% (HPLC) Eact activates the Calcium-activated Chloride channel (CaCC) TMEM16A CaCC. Eact stimulates CaCC conductance in salivary gland cells and submucosal airway epithelial cells. The compound Eact also stimulates submucosal gland secretion in human bronchial tissue and smooth muscle contraction in mouse intestine.
In rat arterial myocytes, Eact [3,4,5-trimethoxy-N-(2-methoxyethyl)-N-(4-phenyl-2-thiazolyl)benzamide] helps to activate chloride current and prevents estradiol synthesis in cultured mouse granulosa cells. It is a small molecule activator of TMEM16A (transmembrane member 16A), that activates TRPV1 (transient receptor potential cation channel subfamily V member 1) and generates pain and itch related symptoms. Eact also initiates endogenous TRPV1 expressed by DRG (dorsal root ganglion) neurons.
I117 R(+)-IAA-94 ≥98% (HPLC), solid Potent Cl- channel blocker.
I8898 Ivermectin Positive allosteric modulator of α7 neuronal nicotinic acetylcholine receptor; also modulates glutamate-GABA-activated chloride channels.
SML1672 JT010 ≥98% (HPLC) JT010 is a non-cytotoxic and highly stable (>90% remains after 2 h in 1 mM DTT or 2-mercaptoethanol) chloroacetamido warhead-carrying thiazole derivative that acts as a potent and TRPA1-selective channel activator via covalent modification of TRPA1 active site Cys621. JT0101 stimulates calcium influx in TRPA1-transfected HEK293 cells in a dose-dependent manner (EC50 = 650 pM) with excellent selectivity over TRPV1, TRPV3, TRPV4, TRPM2, TRPM8, and TRPC5 channels (EC50 >1 μM).
SML1173 Lubiprostone ≥98% (HPLC) Lubiprostone is a bicyclic fatty acid that activates ClC-2 and CFTR chloride channels. Some reports suggest that lubiprostone opens CFTR or both CFTR and ClC-2 through interactions with the prostaglandin receptor EP4. Lubiprostone is used clinically to treat idiopathic chronic constipation and irritible bowel syndrome.
SML0902 MONNA ≥98% (HPLC) MONNA (benzbromarone (Benzb) and N-((4-methoxy)-2-naphthyl)-5-nitroanthranilic acid) is a TMEM16A antagonists. It affects the liberation of sarcoplasmic reticulum (SR) calcium in human airway smooth muscle cells.
MONNA is a TMEM16A (ANO1) calcium-activated chloride channel blocker. MONNA blocks rhTMEM16A (ANO1) channel currents in HEK293 cells with and IC50 of 1.27 μM. The compound MONNA does not affect related human or mouse chloride channels bestrophin-1, CLC2 and CFTR at concentrations up to 10 μM.
N4779 5-Nitro-2-(3-phenylpropylamino)benzoic acid ≥98% Potent chloride channel blocker.
P0024 PG-01 ≥98% (HPLC) CFTR mutations are responsible for cystic fibrosis. The most common mutation is ΔF508, but many others exist. Drugs which can correct channel function of a broad range of CFTR mutants are most desirable for clinical development. PG-01 is a potentiator of ΔF508 (Ka 70 nM) as well as mutants G551D and G1349D (Ka 1100 and 40 nM, respectively). Its broad spectrum may make it more desirable than more mutant-specific CFTR correctors.
SML0493 T16Ainh-A01 ≥95% (HPLC) T16Ainh-A01 is a selective TMEM16A calcium-activated chloride channel inhibitor that strongly inhibits chloride current in salivary gland cells. T16Ainh-A01 poorly inhibited total CaCC current in intestinal and airway epithelial cells, but blocked mainly an initial, agonist-stimulated transient chloride current. T16Ainh-A01 does not alter cytoplasmic calcium and has little effect on CFTR Cl- conductance.
SML1710 Talniflumate ≥98% (HPLC) Talniflumate is a phthalidyl ester of niflumic acid. It acts as an anti-inflammatory molecule and a mucoregulator. Talniflumate is used as a potent therapeutic for cystic fibrosis, chronic obstructive pulmonary disease and asthma. Talniflumate also inhibits the calcium-activated chloride channel hCLCA function, which is involved in mucus overproduction.
Talniflumate is an orally available, potent and selective inhibitor of core mucin-synthesizing enzyme GCNT3 (core 2 b-1,6 N-acetylglucosaminyltransferase). Talniflumate decreases GCNT3 expression and production of mucins in vivo and in vitro. Talniflumate improves responsiveness of pancreatic tumors to gefitinib. Talniflumate is a potent calcium-activated chloride channel (CaCC) blocker.
V2390 VRT-532 ≥98% (HPLC) VRT-532 is a mutated G551D CFTR corrector. VRT-532 mediates G551D-CFTR by enhancement of ATP affinity of the mutant. VRT-532 also potentiates F508del mutated CFTR and works specifically on mutant CFTR rather than other membrane proteins.