|S2623||Omecamtiv mecarbil (CK-1827452)||<1 mg/mL||80 mg/mL||6 mg/mL|
|S7046||Brefeldin A||<1 mg/mL||4 mg/mL||<1 mg/mL|
|S7099||(-)-Blebbistatin||<1 mg/mL||58 mg/mL||<1 mg/mL|
|S2000||Sodium orthovanadate||36 mg/mL||<1 mg/mL||<1 mg/mL|
|S2528||Ciclopirox||<1 mg/mL||42 mg/mL||42 mg/mL|
|S3628||BHQ||<1 mg/mL||10 mg/mL||40 mg/mL|
|S3699||2,3-Butanedione-2-monoxime||20 mg/mL||20 mg/mL||20 mg/mL|
|S3019||Ciclopirox ethanolamine||<1 mg/mL||6 mg/mL||30 mg/mL|
|S2233||Esomeprazole Sodium||73 mg/mL||73 mg/mL||73 mg/mL|
|S7266||Golgicide A||<1 mg/mL||57 mg/mL||4 mg/mL|
|S2222||PF-3716556||<1 mg/mL||79 mg/mL||79 mg/mL|
|S7460||BTB06584||<1 mg/mL||84 mg/mL||<1 mg/mL|
|S8101||CB-5083||<1 mg/mL||82 mg/mL||13 mg/mL|
|S8276||FCCP||<1 mg/mL||50 mg/mL||50 mg/mL|
Omecamtiv mecarbil (CK-1827452) is a specific cardiac myosin activator and a clinical drug for left ventricular systolic heart failure. Phase 2.
Normal and Mutation human iPSC-CMs Structure when Treated with Omecamtiv Mecarbil. Human iPSC-CMs were plated on 100 kPa flat PDMS and grown for five days and left untreated, treated acutely on day 5, or treated continuously from the time of plating with the myosin activator Omecamtiv Mecarbil. iPSC-CMs were then fixed and stained for actin filaments (phalloidin, red) and nucleus (DAPI, blue). (a, c, e) Normal and (b, d, f) Mutation untreated, acutely treated, and continuously treated iPSC-CMs.
Brefeldin A is a lactone antibiotic and ATPase inhibitor for protein transport with IC50 of 0.2 μM in HCT 116 cells, induces cancer cell differentiation and apoptosis.
Cells were treated with brefeldin A or manumycin A, and the resulting supernatant was collected after 48 h for exosomal preparation (lanes 1 and 2), or exosomes obtained from C81 cells were trypsin-treated or freeze/thawed (F/T) and then trypsin-treated (lanes 3 and 4). Lanes 5 and 6, input exosome controls from C81 or CEM cells, respectively. Resulting exosomes were assayed for the presence of Tax by Western blotting.
(-)-Blebbistatin is a cell-permeable inhibitor for non muscle myosin II ATPase with IC50 of ~2 μM in cell-free assays, does not inhibit myosin light chain kinase, inhibits contraction of the cleavage furrow without disrupting mitosis or contractile ring assembly.
(C) MyoIIA inhibition by blebbistatin treatment in vivo impairs leukemia cell extravasation into the brain. One hour before B-ALL cell transfer, C57BL/6 CD45.1+ recipient mice were treated with vehicle or blebbistatin (2.5 mg/kg). Twenty-four hours after B-ALL cell transfer, the recipient mice were intravenously injected with CD19-APC antibodies and then euthanized 4 min later.
Sodium orthovanadate is an alkaline phosphatase and (Na,K)-ATPase inhibitor with IC50 of 10 μM.
Ciclopirox is a broad-spectrum antifungal agent working as an iron chelator.
2,3-Butanedione monoxime (BDM) is the well-characterized, low-affinity, non-competitive inhibitor of skeletal muscle myosin-II that inhibits skeletal and cardiac muscle contraction.
Ciclopirox ethanolamine (Ciclopirox olamine, HOE 296) is a broad-spectrum antifungal agent working as an iron chelator.
Esomeprazole Sodium is a sodium salt of esomeprazole that is a potent proton pump inhibitor with an IC50 of 0.076 mg/kg.
Golgicide A is a potent and rapidly reversible GBF1 inhibitor.
CSFV multiplication was inhibited by GCA. (A) The safe concentration of GCA was tested using the MTT assay. The operations and calculations were the same as those used for BFA. (B) Cellular CSFV RNA with or without 400 nM GCA were examined using real-time PCR. (C) The titers of CSFV with or without GCA were tested by IFA. (D) CSFV proliferation in ST cells with or without GCA was observed by IFA at 24, 48 and 72 hpi. Results from the three independent experiments are shown as means ± SD. *P<0.05 and **P<0.01 compared with the control group.
PF 3716556 is a potent and selective P-CAB (potassium-competitive acid blocker), with pIC50 of 6.026 and 7.095 for the inhibition of porcine H+,K+-ATPase activity in ion-leaky and ion-tight assay, respectively, inhibits gastric acid secretion, displays no activity at Na+,K+-ATPase, used for the treatment of gastroesophageal reflux disease.
BTB06584 is an IF1-dependent, selective inhibitor of the mitochondrial F1 Fo-ATPase.
Changes of mitochondrial membrane potential (ΔΨm). (A) Representative micrographs captured by confocal laser scanning microscope were evaluated for ΔΨm by staining with JC-1 at 24h post ionizing radiation. Red dimers indicated normal mitochondrial function and green monomers indicated collapse of ΔΨm with cytoplasmic fluorescence. Scale bar = 50μm. (B) Kinetics of changes of ΔΨm was showed as the ratio of red to green fluorescence in each treatment staining with JC-1 at 0.5, 6, 12, 24, 48, 72 and 96 h after X-ray radiation (IR) with or without 10μM BTB treatment. Data are expressed as means±SD of triplicate measurements. IR compared with IR+BTB, *p< 0.05, **p< 0.01, t-test. Control compared with IR+BTB, #p< 0.05, ##p< 0.01, t-test.
CB-5083 is a potent, selective, and orally bioavailable p97 AAA ATPase inhibitor with IC50 of 11 nM. Phase 1.
Incubation with VCP inhibitors results in activation of Unfolded Protein Response (UPR). SKOV3 cells were incubated with (C) 2.5 μM CB-5083 for 0, 1, 3, 6, 12, 24 and 48 h. Whole cell lysates were subjected to Western blot analysis and probed for UPR-related proteins
FCCP is a potent uncoupler of oxidative phosphorylation in mitochondria that disrupts ATP synthesis by transporting protons across cell membranes.