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Azilsartan Methyl Ester
CAS No. 147403-52-9
Azilsartan Methyl Ester( —— )
Catalog No. M35894 CAS No. 147403-52-9
Azilsartan Methyl Ester is an angiotensin II receptor antagonist. Azilsartan Methyl Ester inhibits specific binding of [125I]AII (0.2 nM) to bovine adrenal cortex with IC50 value is 0.44uM.
Purity : >98% (HPLC)
COA
Datasheet
HNMR
HPLC
MSDS
Handing Instructions
| Size | Price / USD | Stock | Quantity |
| 50MG | 34 | In Stock |
|
| 100MG | 50 | In Stock |
|
| 500MG | 143 | In Stock |
|
| 1G | Get Quote | In Stock |
|
Biological Information
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Product NameAzilsartan Methyl Ester
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NoteResearch use only, not for human use.
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Brief DescriptionAzilsartan Methyl Ester is an angiotensin II receptor antagonist. Azilsartan Methyl Ester inhibits specific binding of [125I]AII (0.2 nM) to bovine adrenal cortex with IC50 value is 0.44uM.
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DescriptionAzilsartan methyl ester, a derivative of Azilsartan (HY-14914), is an angiotensin II receptor antagonist that plays an important role in hypertension.
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In Vitro——
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In Vivo——
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Synonyms——
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PathwayEndocrinology/Hormones
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TargetRAAS
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RecptorRAAS
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Research Area——
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Indication——
Chemical Information
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CAS Number147403-52-9
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Formula Weight470.48
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Molecular FormulaC26H22N4O5
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Purity>98% (HPLC)
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Solubility——
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SMILESCCOc1nc2cccc(C(=O)OC)c2n1Cc1ccc(cc1)-c1ccccc1-c1nc(=O)o[nH]1
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Chemical Name——
Shipping & Storage Information
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Storage(-20℃)
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ShippingWith Ice Pack
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Stability≥ 2 years
Reference
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Voglibose
Voglibose, an N-substituted derivative of valiolamine, exhibits excellent inhibitory activity against α-glucosidases and action against hyperglycemia and various disorders caused by hyperglycemia.
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Telmisartan
Telmisartan is an angiotensin II receptor antagonist (ARB) used in the management of hypertension.
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N-Acetyl-Ser-Asp-Lys...
Acetyl Ser-Asp-Lys-Pro is formed in bone marrow cells by enzymatic processing of thymosin β4. It inhibits the entry of pluripotent hemopoietic stem cells into S-phase of the cell cycle and protects against Ara-C lethality in mice.N-Acetyl-Ser-Asp-Lys-Pro (AcSDKP) is a specific substrate for the N-terminal site of ACE and increases 5-fold during ACE inhibitor therapy.??AcSDKP inhibited the proliferation of isolated cardiac fibroblasts (P<0.05) but significantly stimulated the proliferation of vascular smooth muscle cells.?
