atp release

Sambutoxin, a new mycotoxin produced by toxic Fusarium isolates obtained from rotted potato tubers, it can cause toxic effects in rats, including body weight loss, feed refusal, hemorrhage in the stomach and intestines, and, finally, death when rats were

Aglafoline inhibits in a concentration-dependent manner the aggregation and ATP release reaction induced in washed rabbit platelets by PAF (platelet-activating factor). The IC50 values of Aglafoline on PAF (3.6 nM)-induced platelet aggregation were about 50 μM.

Dibutyryl-cGMP sodium (Bt2cGMP sodium) is a cell-permeable cGMP analog that preferentially activates cGMP-dependent protein kinase (PKG). It inhibits [3H]-arachidonic acid release in human platelets stimulated by gamma thrombin and can induce peripheral analgesia by activating ATP-sensitive K+ channels.

Myosin V-IN-1 is a potent and selective inhibitor of Myosin V with a Ki value of 6 μM.Myosin V-IN-1 inhibits actin V and slows down actin-activated myosin V ATPase by selectively inhibiting the release of ADP from the actinoglobulin complex.

Salbutamol (Albuterol) stimulates beta2-adrenergic receptors in the lungs, thereby activating the enzyme adenylate cyclase that catalyzes the conversion of ATP to cyclic-3', 5'-adenosine monophosphate (cAMP). Salbutamol Sulfate is the sulfate salt of the short-acting sympathomimetic agent albuterol, a 1:1 racemic mixture of (R)-albuterol and (S)-albuterol with bronchodilator activity. Increased cAMP concentrations relax the bronchial smooth muscle, relieve bronchospasms, and reduce inflammatory cell mediator release, especially from mast cells. To a lesser extent, Salbutamol stimulates beta1-adrenergic receptors, thereby increasing the force and rate of myocardial contraction.

TNKS-2-IN-1 is a TNKS-2 inhibitor.TNKS-2-IN-1 inhibits TNKS-1 and TNKS-2 with IC50s of 259 nM and 1100 nM, respectively.TNKS-2-IN-1 has antimicrobial activity against E. coli and S. aureus.TNKS-2-IN-1 inhibits the release of IL-1β from the NLRP3 inflammasome (IC50: 5 μM) by inhibiting IL-1β release from ATP-stimulated J1A.774 cells.

Gliclazide (SE1702), an oral antihyperglycemic agent, belongs to the sulfonylurea class of insulin secretagogues, which act by stimulating beta-cells of the pancreas to release insulin.

Tpl2 Kinase Inhibitor 1 is a potent, reversible, and highly selective ATP-competitive inhibitor of Tpl2 (MAP3K8/COT) serine/threonine kinase, with an IC₅₀ of 50 nM for Tpl2 kinase inhibition. In vitro, Tpl2 Kinase Inhibitor 1 inhibits LPS-induced TNF-α release from human primary monocytes (IC₅₀ = 0.7 μM). Tpl2 Kinase Inhibitor 1 can be used in research on inflammatory responses and certain cancers.

P2X4 antagonist-4 (compound 64) is a potent P2X4R antagonist with an IC50 value of 8 µM. It can inhibit ATP-induced activation of the NLRP3 inflammasome and the subsequent release of IL-1β.

GAT2711 is a full agonist of α9nAChR, with an EC50 of 230 nM. It exhibits 340 times greater selectivity for α9 over α7nAChR. In THP-1 cells, GAT2711 inhibits ATP-induced IL-1β release. Additionally, GAT2711 retains full analgesic activity in α7nAChR knockout mice.

NLRP3/URAT1-IN-1 is an orally active dual inhibitor targeting NLRP3 and URAT1, with an IC50 of 3.81 μM. It suppresses IL-1β release in mouse bone marrow-derived macrophages (BMDMs) stimulated by LPS and ATP, with an IC50 of 2.61 μM. Additionally, NLRP3/URAT1-IN-1 decreases serum uric acid (SUA) levels and alleviates liver/kidney injury in mice with acute hyperuricemia (HUA). This compound is relevant for research on gout and hyperuricemia.

NLRP3-IN-84 (Compound 32) is an inhibitor of the NLRP3 inflammasome. It interferes with the oligomerization of NLRP3 by inhibiting the activity of NLRP3ATPase (IC50= 158.4 nM). NLRP3-IN-84 also inhibits Caspase-1 (IC50= 27.7 nM), the release of IL-1β in PBMC (IC50= 19.5 nM) and mPBMC (IC50= 24.2 nM), and ASC speck formation (IC50= 131 nM). It shows no inhibitory activity against the NLRC4 and AIM2 inflammasomes. NLRP3-IN-84 exhibits significant in vivo anti-inflammatory effects in a mouse acute peritonitis model, making it useful for studying NLRP3-related inflammatory diseases.

Bimakalim (EMD-52692) is an opener of ATP-sensitive potassium channels. It can decrease MPO (myeloperoxidase) activity across the wall and mimics the effects of ischemic preconditioning by reducing infarct size, adenosine release, and neutrophil function in dogs.

2DG-ODDA is a potent antitumor derivative of 2-deoxyglucose (2-DG). It induces apoptosis and reduces ATP production. 2DG-ODDA is absorbed via fatty acid and glucose transporters and cleaved by α-Mannosidase to release 2DG, thereby inhibiting N-glycosylation and disrupting cellular metabolism. It suppresses tumor growth in 4T1 murine models and is applicable in triple-negative breast cancer (TNBC) research.

nAChRantagonist 2 is a selective nAChR antagonist that demonstrates inhibitory activity against nAChR subtypes, including human α9α10, α9, and α7, in Xenopus laevis oocytes, with IC50 values of 16.0 nM, 26.2 nM, and 336.3 nM, respectively. It inhibits ATP-induced IL-1β release at nanomolar concentrations and can be utilized in research related to non-opioid analgesics and immunomodulators.

Ganglioside GM1 asialo is a component of cellular lipid rafts and can be formed by the cleavage of the sialic acid residue from ganglioside GM1 by neuraminidase. Ganglioside GM1 asialo is a glycolipid receptor for P. aeruginosa flagellin and stimulates defensive responses in host cells, including extracellular ATP release, calcium mobilization, and ERK1/2 phosphorylation when stimulated by flagellin and an anti-ganglioside GM1 asialo antibody. The percentage of ganglioside GM1 asialo-positive natural killer (NK) and CD8+ T cells in lung is increased in a mouse model of respiratory syncytial virus (RSV) infection compared with healthy animals. Depletion of ganglioside GM1 asialo-positive NK and T cells reduces IFN-γ levels in the lung, reduces weight loss, and increases lung viral load in RSV-infected mice. Ganglioside GM1 asialo mixture contains ganglioside GM1 asialo molecular species with C18:1 and C20:1 sphingoid backbones.

ITH15004 is a non-nucleotide antagonist of the purinergic P2X7receptor (IC50= 9 μM in HEK293 cells expressing the human receptor).1It inhibits ATP-induced currents inX. laevisoocytes expressing the human P2X7receptor when used at a concentration of 100 μM. ITH15004 (1 μM) decreases IL-1β release from LPS-primed, ATP-stimulated isolated mouse peritoneal macrophages. It has high permeability in a parallel artificial membrane permeability assay (PAMPA). 1.Calzaferri, F., Narros-Fernández, P., de Pascual, R., et al.Synthesis and pharmacological evaluation of novel non-nucleotide purine derivatives as P2X7 antagonists for the treatment of neuroinflammationJ. Med. Chem.64(4)2272-2290(2021)

JC-171, a selective inhibitor of the NLRP3 inflammasome, effectively inhibits LPS/ATP-induced interleukin-1β (IL-1β) release from J774A.1 macrophages with an IC50 of 8.45 μM[1].

Potent NLRP3 inflammasome inhibitor (IC50 = 60-80 nM). Inhibits nigericin- and ATP-induced IL-1β release. Baldwin et al (2017) Boron-Based Inhibitors of the NLRP3 Inflammasome. Cell Chem.Biol. 24 1321 PMID:28943355 |Redondo-Castro et al (2018) Development of a characterised tool kit for the interrogation of NLRP3 inflammasome-dependent responses. Sci.Rep. 8 5667 PMID:29618797

TAT-Gap19(I130A) is a control peptide for TAT-Gap19, a Cx43 hemichannel blocker. TAT-Gap19(I130A) consists of TAT-GAP19 with a I130A amino acid residue change at a key residue for GAP19 activity. In C6 glioma cells expression Cx43, TAT-GAP19(1130A) does not inhibit [Ca2+]i-triggered ATP release at 200 μM. TAT-Gap19(I130A) is cell permeable.

AZ-DF 265 is a hypoglycaemic drug which stimulates insulin release. AZ-DF-265 inhibits ATP-sensitive potassium channels and displaces [3H]-glibenclamide from the sulphonylurea receptor.

GSK1370319A is a potent P2X7 antagonist (IC50 = 3.2 nM). GSK1370319A inhibits ATP-induced increase in IL-1β release and caspase 1 activation in lipopolysaccharide (LPS)-primed mixed glia by blocking assembly of the inflammasome in a pannexin 1-dependent manner. GSK1370319A also inhibits ATP-induced subregion-specific neuronal loss in hippocampal organotypic slice cultures, which is dependent on its ability to prevent inflammasome assembly in glia. Significantly, GSK1370319A attenuates age-related deficits in long-term potentiation (LTP) and inhibits the accompanying age-related caspase 1 activity. We conclude that inhibiting P2X(7) receptor-activated NLRP3 inflammasome formation and the consequent IL-1β release from glia preserve neuronal viability and synaptic activity.

Dimethyl L-glutamate (Dimethyl glutamate), a membrane-permeable derivative of glutamate, stimulates glucose-induced insulin release, suppresses K_ATP channel activities, inhibits E. gracilis growth, and causes abnormal cell division. This compound is utilized in diabetes research, focusing on glucose transport, phosphorylation, and metabolism.

Thapsigargicin is a sesquiterpene lactone natural product isolated from the poisonous plant Thapsia garganica. Thapsigargicin is a potent non-competitive inhibitor of the sarcoplasmic reticulum/endoplasmic reticulum calcium ATPase (SERCA)(IC₅₀ ≈ 10–30 nM). By specifically blocking the SERCA pump, it depletes endoplasmic reticulum calcium stores and elevates cytoplasmic calcium levels, thereby activating mast cells and leukocytes to release histamine, inducing endoplasmic reticulum stress and apoptosis. Thapsigargicin can be used in studies of calcium signaling pathways and inflammatory responses.