HA-130 - CAS 1229652-21-4
Catalog number: 1229652-21-4
Category: Inhibitor
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Molecular Formula:
C24H19BFNO5S
Molecular Weight:
463.29
COA:
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Targets:
Phosphodiesterase (PDE)
Description:
HA-130, an effective autotaxin (ATX) inhibitor, has been found to restrain the cell migration related to ATX in in an A2058 melanoma cells. IC50: 28 nM.
Purity:
>98 %
Appearance:
Powder
Synonyms:
SCHEMBL1555945; 1229652-21-4; HA130; HA-130; HA 130.
Solubility:
10 mM in DMSO
Storage:
-20ºC Freeze
MSDS:
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Application:
HA-130 is an effective autotaxin (ATX) inhibitor that has been found to restrain the cell migration related to ATX in in an A2058 melanoma cells.
Shelf Life:
As supplied, 2 years from the QC date provided on the Certificate of Analysis, when stored properly
Quantity:
Milligrams-Grams
InChIKey:
VTNKMYWFWQTEHE-UHFFFAOYSA-N
InChI:
InChI=1S/C24H19BFNO5S/c26-20-8-4-17(5-9-20)14-27-23(28)22(33-24(27)29)13-16-6-10-21(11-7-16)32-15-18-2-1-3-19(12-18)25(30)31/h1-13,30-31H,14-15H2
Canonical SMILES:
B(C1=CC(=CC=C1)COC2=CC=C(C=C2)C=C3C(=O)N(C(=O)S3)CC4=CC=C(C=C4)F)(O)O
1.Curative effect of neutral macroporous resin hemoperfusion on treating hemodialysis patients with refractory uremic pruritus.
Li WH;Yin YM;Chen H;Wang XD;Yun H;Li H;Luo J;Wang JW Medicine (Baltimore). 2017 Mar;96(12):e6160. doi: 10.1097/MD.0000000000006160.
This study aims to investigate the efficacy and safety of neutral macroporous resin hemoperfusion in treating maintenance hemodialysis (MHD) patients with refractory uremic pruritus (RUP).Ninety patients were enrolled and were randomly divided into 3 groups: control group, experiment 1 group, and experiment 2 group. Clinical symptom scores of skin itching were recorded before and at 4 and 8 weeks after the treatment. In addition, serum parathyroid hormone (PTH), calcium (Ca), phosphorus (P), and C-reactive protein (CRP) were detected; and the calcium-phosphorus product ([Ca] × [P]) was calculated to compare the curative effect.VSA score, modified Duo pruritus score, and CRP: these indices decreased to some extent at 4 and 8 weeks after treatment in the 2 experiment groups, compared with pretreatment (P < 0.05); and differences among these 3 groups were statistically significant (P < 0.05). PTH, P, and [Ca] × [P]: these indices decreased to some extent at 4 and 8 weeks after treatment in the 2 experiment groups, compared with pretreatment (P < 0.05); and differences between the control and experiment 1 groups, as well as between the control and experiment 2 groups, were statistically significant (P < 0.
2.Lysophosphatidylethanolamine utilizes LPA(1) and CD97 in MDA-MB-231 breast cancer cells.
Park SJ;Lee KP;Kang S;Chung HY;Bae YS;Okajima F;Im DS Cell Signal. 2013 Nov;25(11):2147-54. doi: 10.1016/j.cellsig.2013.07.001. Epub 2013 Jul 6.
Lysophosphatidylethanolamine (LPE) is a lyso-type metabolite of phosphatidylethanolamine (a plasma membrane component), and its intracellular Ca(2+) ([Ca(2+)]i) increasing actions may be mediated through G-protein-coupled receptor (GPCR). However, GPCRs for lysophosphatidic acid (LPA), a structurally similar representative lipid mediator, have not been implicated in LPE-mediated activities in SK-OV3 or OVCAR-3 ovarian cancer cells or in receptor over-expression systems. In the present study, LPE-induced [Ca(2+)]i increase was observed in MDA-MB-231 cells but not in other breast cancer cell lines. In addition, LPE- and LPA-induced responses showed homologous and heterologous desensitization. Furthermore, VPC32183 and Ki16425 (antagonists of LPA1 and LPA3) inhibited LPE-induced [Ca(2+)]i increases, and knockdown of LPA1 by transfection with LPA1 siRNA completely inhibited LPE-induced [Ca(2+)]i increases. Furthermore, the involvement of CD97 (an adhesion GPCR) in the action of LPA1 in MDA-MB-231 cells was demonstrated by siRNA transfection. Pertussis toxin (a specific inhibitor of Gi/o proteins), edelfosine (an inhibitor of phospholipase C), or 2-APB (an inhibitor of IP3 receptor) completely inhibited LPE-induced [Ca(2+)]i increases, whereas HA130, an inhibitor of autotaxin/lysophospholipase D, did not.
3.The phospholipase A2 activity of peroxiredoxin 6 modulates NADPH oxidase 2 activation via lysophosphatidic acid receptor signaling in the pulmonary endothelium and alveolar macrophages.
Vázquez-Medina JP;Dodia C;Weng L;Mesaros C;Blair IA;Feinstein SI;Chatterjee S;Fisher AB FASEB J. 2016 Aug;30(8):2885-98. doi: 10.1096/fj.201500146R. Epub 2016 May 13.
Peroxiredoxin 6 (Prdx6) is essential for activation of NADPH oxidase type 2 (NOX2) in pulmonary microvascular endothelial cells (PMVECs), alveolar macrophages (AMs), and polymorphonuclear leukocytes. Angiotensin II and phorbol ester increased superoxide/H2O2 generation in PMVECs, AMs, and isolated lungs from wild-type (WT) mice, but had much less effect on cells or lungs from Prdx6-null or Prdx6-D140A-knock-in mice that lack the phospholipase A2 activity (PLA2) of Prdx6; addition of either lysophosphatidylcholine (LPC) or lysophosphatidic acid (LPA) to cells restored their oxidant generation. The generation of LPC by PMVECs required Prdx6-PLA2 We propose that Prdx6-PLA2 modulates NOX2 activation by generation of LPC that is converted to LPA by the lysophospholipase D activity of autotaxin (ATX/lysoPLD). Inhibition of lysoPLD with HA130 (cells,10 μM; lungs, 20 μM; IC50, 29 nM) decreased agonist-induced oxidant generation. LPA stimulates pathways regulated by small GTPases through binding to G-protein-coupled LPA receptors (LPARs). The LPAR blocker Ki16425 (cells, 10 μM; lungs, 25 μM; Ki, 0.34 μM) or cellular knockdown of LPAR type 1 decreased oxidant generation and blocked translocation of rac1 to plasma membrane.
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CAS 1229652-21-4 HA-130

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