DC Chemicals' products qualify for U.S. tariff exemptions. We guarantee no price increases due to customs duties and maintain stable supply, continuing to deliver reliable research solutions to our American clients.
| Cas No.: | 177036-94-1 |
| Chemical Name: | (S)-2-(4,6-Dimethylpyrimidin-2-yloxy)-3-methoxy-3,3-diphenylpropanoic acid |
| Synonyms: | (S)-2-(4,6-Dimethylpyrimidin-2-yloxy)-3-methoxy-3,3-diphenylpropanoic acid;BSF 208075,(+)-(2S)-2-[(4,6-DIMETHYLPYRIMIDIN-2-YL)OXY]-3-METHOXY-3,3-DIPHENYLPROPANOIC ACID;AMBRISENTAN;2-(4,6-Dimethylpyrimidin-2-yl)oxy-3-methoxy-3,3-di(phenyl)propanoic acid;(aS)-a-[(4,6-Dimethyl-2-pyrimidinyl)oxy]--methoxy--phenylbenzenepropanoic Acid;BSF 208075;LU 208075;(+-)-(2S)-2-((4,6-Dimethylpyrimidin-2-yl)oxy)-3-methoxy-3,3-diphenylpropanoic acid,bsf-208075;(2S)-2-(4,6-dimethylpyrimidin-2-yl)oxy-3-methoxy-3,3-diphenylpropanoic acid;(S)-2-((4,6-Dimethylpyrimidin-2-yl)oxy)-3-methoxy-3,3-diphenylpropanoic acid;BSF-208075;Letairis;LU-208075;UNII-HW6NV07QEC;(+)-(2S)-2-[(4,6-dimethylpyrimidin-2-yl)oxy]-3-methoxy-3,3-diphenylpropanoic acid;(S)-2-[(4,6-Dimethylpyrimidin-2-yl)oxy]-3-methoxy-3,3-diphenylpropionic Acid;Ambrisentan Tablets;(R,S)-AMbrisentan-d5;LU-208075,BSF-208075;ambrisentan,CID 6918493;AMbrisentan (BSF 208075) |
| SMILES: | O=C([C@H](C(OC)(C1=CC=CC=C1)C2=CC=CC=C2)OC3=NC(C)=CC(C)=N3)O |
| Formula: | C22H22N2O4 |
| M.Wt: | 378.42108 |
| Purity: | >99% |
| Sotrage: | 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO |
| Description: | Ambrisentan is a selective ET type A receptor (ETAR) antagonist. |
| In Vivo: | In the Ambrisentan group, hepatic hydroxyproline content is significantly lower than in the control group (18.0 μg/g±6.1 μg/g vs 33.9 μg/g±13.5 μg/g liver, respectively, P=0.014). Hepatic fibrosis estimated by Sirius red staining and areas positive for α-smooth muscle actin, indicative of activated hepatic stellate cells, are also significantly lower in the Ambrisentan group (0.46%±0.18% vs 1.11%±0.28%, respectively, P=0.0003; and 0.12%±0.08% vs 0.25%±0.11%, respectively, P=0.047). Moreover, hepatic RNA expression levels of procollagen-1 and tissue inhibitor of metalloproteinase-1 (TIMP-1) are significantly lower by 60% and 45%, respectively, in the Ambrisentan group. Inflammation, steatosis, and endothelin-related mRNA expression in the liver are not significantly different between the groups. Ambrisentan attenuates the progression of hepatic fibrosis by inhibiting hepatic stellate cell activation and reducing procollagen-1 and TIMP-1 gene expression. Ambrisentan did not affect inflammation or steatosis[1]. |
| In Vitro: | Ambrisentan is an endothelin type A receptor antagonist[1]. Ambrisentan induces Nrf2 activation. Endothelial permeability increased in BMEC monolayers at 24 h of hypoxia exposure and compared to vehicle control, Ambrisentan attenuates hypoxia-induced BMEC leak. These results are reversed when prior to treatment BMEC are transfected with siRNA against Nrf2[2]. |
| Cell Assay: | Unless otherwise stated, for each BMEC experiment cells are randomly divided into 4 groups: (1) normoxia vehicle control (Nx-CTRL); (2) normoxia-treated; (3) hypoxia (24 h) control (Hx-CTRL) and (4) hypoxia (24 h) treated. As previously described, Nrf2 activators are added 24 h prior to any hypoxic exposures. Cell treatments are; Protandim (100 μg/mL), methazolamide (125 μg/mL, nifedipine (7 μg/mL) or Ambrisentan (40 μg/mL). In addition, some cells are treated with Nrf2 siRNA. In these experiments, siRNA is added 24 h prior to drug treatments. The rationale for 24 h hypoxia exposure for BMEC is to ensure that cells remained transfected with siRNA for the pre-treatment of drugs (24 h in normoxia) and during the 24 h hypoxia exposure. Data is collected from at least three separate cell culture preparations on three separate days (n=9)[2]. |
| Animal Administration: | Unless otherwise stated, for each BMEC experiment cells are randomly divided into 4 groups: (1) normoxia vehicle control (Nx-CTRL); (2) normoxia-treated; (3) hypoxia (24 h) control (Hx-CTRL) and (4) hypoxia (24 h) treated. As previously described, Nrf2 activators are added 24 h prior to any hypoxic exposures. Cell treatments are; Protandim (100 μg/mL), methazolamide (125 μg/mL, nifedipine (7 μg/mL) or Ambrisentan (40 μg/mL). In addition, some cells are treated with Nrf2 siRNA. In these experiments, siRNA is added 24 h prior to drug treatments. The rationale for 24 h hypoxia exposure for BMEC is to ensure that cells remained transfected with siRNA for the pre-treatment of drugs (24 h in normoxia) and during the 24 h hypoxia exposure. Data is collected from at least three separate cell culture preparations on three separate days (n=9)[2]. |
| References: | Unless otherwise stated, for each BMEC experiment cells are randomly divided into 4 groups: (1) normoxia vehicle control (Nx-CTRL); (2) normoxia-treated; (3) hypoxia (24 h) control (Hx-CTRL) and (4) hypoxia (24 h) treated. As previously described, Nrf2 activators are added 24 h prior to any hypoxic exposures. Cell treatments are; Protandim (100 μg/mL), methazolamide (125 μg/mL, nifedipine (7 μg/mL) or Ambrisentan (40 μg/mL). In addition, some cells are treated with Nrf2 siRNA. In these experiments, siRNA is added 24 h prior to drug treatments. The rationale for 24 h hypoxia exposure for BMEC is to ensure that cells remained transfected with siRNA for the pre-treatment of drugs (24 h in normoxia) and during the 24 h hypoxia exposure. Data is collected from at least three separate cell culture preparations on three separate days (n=9)[2]. |
MSDS
COA
| LOT NO. | DOWNLOAD |
|
|
|
| 2018-0101 |
|
| 2018-0101 |
|